The document provides an overview of the immune system and autoimmune disorders. It discusses the organs and cells involved in immunity, including T cells, B cells, macrophages, and neutrophils. It describes innate and acquired immunity. Types of autoimmune disorders mentioned include rheumatoid arthritis and systemic lupus erythematosus. Key symptoms, diagnostic tests, and medical management are outlined for these conditions. Nursing interventions focus on promoting comfort, self-care, education, and adapting to life with a chronic condition.
Primary immunodeficiencies are caused by genetic defects that impair the immune system's ability to fight infections. They can be classified as humoral, affecting antibody production; cellular, affecting T cells and cell-mediated immunity; or combined. Common primary immunodeficiencies include X-linked agammaglobulinemia, isolated IgA deficiency, common variable immunodeficiency, hyper IgM syndrome, and severe combined immunodeficiency. Secondary immunodeficiencies are acquired, having underlying causes like infections, malnutrition, aging, or drugs. Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV).
The document discusses immune responses and immune-related diseases. It covers four types of diseases that can result from issues with the immune system: 1) inadequate immune response (immunodeficiency), 2) inappropriate immune response (autoimmune diseases and graft rejection), 3) excessive immune response (hypersensitivity), and 4) amyloidosis. It provides examples and details of primary and secondary immunodeficiencies, transplant rejection, autoimmune diseases, HIV/AIDS, and opportunistic infections seen in AIDS patients.
This document discusses autoimmunity and provides examples of several autoimmune diseases. It begins by defining autoimmunity as an inappropriate immune response directed against self-components. It then discusses how failure to eliminate self-reactive lymphocytes during development can lead to autoimmunity. Several autoimmune diseases are described in detail, including the mechanisms, symptoms, and treatments. Animal models of autoimmune diseases are also discussed.
This document discusses autoimmunity, including:
- What autoimmunity is, the history of its discovery, and proposed mechanisms. Mechanisms include sequestered antigens, escape of autoreactive clones, loss of regulatory T cells, cross-reactive antigens, and altered self antigens.
- Types of autoimmune diseases classified by organ specificity, systemic diseases, pathogenic organisms involved, and type of hypersensitivity reaction. Examples are given for each category.
- Laboratory diagnosis of autoimmune diseases including routine tests, autoantibodies like ANA and RF, acute phase proteins, and HLA typing. Specific autoantibody patterns are shown.
- Treatment approaches including symptomatic treatments and immunosuppressive agents like ant
The document summarizes a chapter about autoimmunity and autoimmune diseases from three perspectives:
1) It outlines several key autoimmune diseases, their causes from abnormal immune responses against self-antigens, and their symptoms.
2) It discusses the use of animal models to study the mechanisms and potential treatments of autoimmune diseases.
3) It examines current therapeutic approaches that aim to suppress autoimmune responses through drugs or removal of target organs, and potential alternative strategies like inducing tolerance to self-antigens.
Autoimmune diseases occur when the immune system mistakenly attacks and damages healthy body tissues. There are over 80 types of autoimmune diseases, including rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus. The causes are not fully understood but may involve genetic and environmental factors. Common treatments aim to suppress the immune system to reduce symptoms, though diagnosis and treatment can be challenging given the wide variation in symptoms and tissues affected across different autoimmune diseases.
The document discusses different types of immune disorders:
1. Hypersensitivity reactions (allergies) are caused by an exaggerated immune response upon re-exposure to an antigen and are classified into four types.
2. Autoimmune diseases occur when the immune system attacks the body's own tissues.
3. Immunodeficiency diseases result from inadequate immune response.
4. Amyloidosis involves abnormal protein buildup in tissues.
This document discusses the role of infections in triggering or exacerbating autoimmune diseases. It outlines four main mechanisms by which this can occur: molecular mimicry, epitope spreading, bystander activation, and exposure of cryptic antigens. Several examples of specific pathogens and the autoimmune diseases they may relate to are described in detail, including evidence from human studies and animal models. While links between certain infections and autoimmunity exist, direct evidence is still limited. Defining genetic risk factors may help understand disease pathogenesis in cases with a suspected infectious trigger.
Primary immunodeficiencies are caused by genetic defects that impair the immune system's ability to fight infections. They can be classified as humoral, affecting antibody production; cellular, affecting T cells and cell-mediated immunity; or combined. Common primary immunodeficiencies include X-linked agammaglobulinemia, isolated IgA deficiency, common variable immunodeficiency, hyper IgM syndrome, and severe combined immunodeficiency. Secondary immunodeficiencies are acquired, having underlying causes like infections, malnutrition, aging, or drugs. Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV).
The document discusses immune responses and immune-related diseases. It covers four types of diseases that can result from issues with the immune system: 1) inadequate immune response (immunodeficiency), 2) inappropriate immune response (autoimmune diseases and graft rejection), 3) excessive immune response (hypersensitivity), and 4) amyloidosis. It provides examples and details of primary and secondary immunodeficiencies, transplant rejection, autoimmune diseases, HIV/AIDS, and opportunistic infections seen in AIDS patients.
This document discusses autoimmunity and provides examples of several autoimmune diseases. It begins by defining autoimmunity as an inappropriate immune response directed against self-components. It then discusses how failure to eliminate self-reactive lymphocytes during development can lead to autoimmunity. Several autoimmune diseases are described in detail, including the mechanisms, symptoms, and treatments. Animal models of autoimmune diseases are also discussed.
This document discusses autoimmunity, including:
- What autoimmunity is, the history of its discovery, and proposed mechanisms. Mechanisms include sequestered antigens, escape of autoreactive clones, loss of regulatory T cells, cross-reactive antigens, and altered self antigens.
- Types of autoimmune diseases classified by organ specificity, systemic diseases, pathogenic organisms involved, and type of hypersensitivity reaction. Examples are given for each category.
- Laboratory diagnosis of autoimmune diseases including routine tests, autoantibodies like ANA and RF, acute phase proteins, and HLA typing. Specific autoantibody patterns are shown.
- Treatment approaches including symptomatic treatments and immunosuppressive agents like ant
The document summarizes a chapter about autoimmunity and autoimmune diseases from three perspectives:
1) It outlines several key autoimmune diseases, their causes from abnormal immune responses against self-antigens, and their symptoms.
2) It discusses the use of animal models to study the mechanisms and potential treatments of autoimmune diseases.
3) It examines current therapeutic approaches that aim to suppress autoimmune responses through drugs or removal of target organs, and potential alternative strategies like inducing tolerance to self-antigens.
Autoimmune diseases occur when the immune system mistakenly attacks and damages healthy body tissues. There are over 80 types of autoimmune diseases, including rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus. The causes are not fully understood but may involve genetic and environmental factors. Common treatments aim to suppress the immune system to reduce symptoms, though diagnosis and treatment can be challenging given the wide variation in symptoms and tissues affected across different autoimmune diseases.
The document discusses different types of immune disorders:
1. Hypersensitivity reactions (allergies) are caused by an exaggerated immune response upon re-exposure to an antigen and are classified into four types.
2. Autoimmune diseases occur when the immune system attacks the body's own tissues.
3. Immunodeficiency diseases result from inadequate immune response.
4. Amyloidosis involves abnormal protein buildup in tissues.
This document discusses the role of infections in triggering or exacerbating autoimmune diseases. It outlines four main mechanisms by which this can occur: molecular mimicry, epitope spreading, bystander activation, and exposure of cryptic antigens. Several examples of specific pathogens and the autoimmune diseases they may relate to are described in detail, including evidence from human studies and animal models. While links between certain infections and autoimmunity exist, direct evidence is still limited. Defining genetic risk factors may help understand disease pathogenesis in cases with a suspected infectious trigger.
The document discusses disorders of the immune system. It describes the functions of a normal immune system and what can go wrong, including immunodeficiencies where the immune system is weak or overactive. It covers specific immune disorders like allergies, autoimmune diseases, and transplant rejection. It also discusses cancer immunology and HIV/AIDS.
The document discusses the molecular mechanisms of autoimmunity, including molecular mimicry, superantigens, epitope spreading, inappropriate MHC expression, polyclonal B cell activation by viruses and bacteria, and cytokine dysregulation. It also covers genes associated with autoimmunity, environmental factors like drugs and toxins, and sex differences in autoimmune diseases.
This document provides an overview of autoimmune diseases including causes, types, links to HLA genes, treatment approaches, and mouse models. It discusses three main types of autoimmune diseases: haemolytic, localized, and systemic. Examples like Hashimoto's thyroiditis, myasthenia gravis, multiple sclerosis, type 1 diabetes, systemic lupus erythematosus, and rheumatoid arthritis are explained. The roles of HLA genes and immunosuppressive drugs in treatment are also summarized. Mouse models that replicate human autoimmune conditions are noted.
This document provides information on autoimmune disorders, including:
- Causes of autoimmunity include sequestered antigens, altered antigens, loss of immunoregulation, and loss of self-tolerance.
- Common autoimmune diseases discussed include systemic lupus erythematosus and systemic sclerosis.
- For systemic lupus erythematosus, clinical manifestations, etiology, pathology, and treatment are summarized. Oral manifestations including bleeding and ulcers are also noted.
- Systemic sclerosis causes fibrosis of the skin, subcutaneous tissue, muscles and internal organs. Its etiology is unclear but involves genetic and environmental factors.
This document discusses autoimmunity and its underlying mechanisms. Autoimmunity occurs when the immune system mistakenly attacks and destroys healthy body tissue. The immune system normally distinguishes self from non-self through mechanisms of central and peripheral tolerance that eliminate or inactivate self-reactive immune cells. A defect or breakdown in these tolerance mechanisms can lead to autoimmunity. Specific mechanisms that may cause this include exposure of normally hidden self-antigens, antigen alteration, molecular mimicry between foreign and self-antigens, emergence of forbidden self-reactive clones, and defects in regulatory T cells or other immune cells. Common autoimmune diseases are then classified as hematological, organ-specific, or systemic.
Autoimmunity occurs when the immune system loses tolerance to its own tissues and mounts an immune response against them. There are several potential mechanisms for this loss of tolerance, including molecular mimicry between foreign and self antigens, sequestered self antigens being exposed to the immune system, and failures of regulatory mechanisms that normally suppress autoreactive immune cells. Autoimmune diseases result when this autoreactivity causes tissue damage. Examples include diseases caused by autoantibodies like rheumatoid arthritis, Graves' disease, and Hashimoto's thyroiditis, as well as those caused by autoreactive T cells like multiple sclerosis and insulin-dependent diabetes.
Autoimmunity results from a failure of the immune system to distinguish self from non-self. There are several mechanisms that can cause this including genetic factors, immunological issues, and infections. Autoimmune diseases can be organ-specific, where autoantibodies attack a single organ, or non-organ specific which causes systemic damage. Common autoimmune diseases include systemic lupus erythematosus, rheumatoid arthritis, myasthenia gravis, and Sjogren's syndrome. Tissue damage in autoimmune diseases is typically caused by type II or type III hypersensitivity reactions.
This document discusses autoimmunity, including its definition as an inappropriate immune response against self cells/tissues due to self-tolerance failure. Various triggers are described, such as genetic factors like certain HLA alleles associated with diseases, environmental factors like molecular mimicry between pathogens and self-antigens, and non-genetic host factors including immunodeficiencies. Numerous autoimmune diseases are detailed along with their antibody targets and clinical features. Diagnosis involves clinical exams, labs to detect autoantibodies, and biopsies. Treatment focuses on reducing inflammation through steroids, blocking cytokines/integrins/B cells, or more extreme measures like immunosuppressants.
Autoimmunity occurs when the immune system mistakenly attacks and damages normal body tissues. There are several proposed mechanisms for how this occurs, including molecular mimicry between foreign and self-antigens. Autoimmune diseases can be organ-specific like Hashimoto's thyroiditis or systemic. Women are more susceptible than men potentially due to immune response differences, sex hormones, and genetics like two X chromosomes carrying immune genes. Treatment may involve modulating immune responses through vaccines, monoclonal antibodies, or inducing tolerance with oral antigens.
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
Your body's immune system protects you from disease and infection. But if you have an autoimmune disease, your immune system attacks healthy cells in your body by mistake. Autoimmune diseases can affect many parts of the body.
No one is sure what causes autoimmune diseases. They do tend to run in families. Women - particularly African-American, Hispanic-American, and Native-American women - have a higher risk for some autoimmune diseases.
There are more than 80 types of autoimmune diseases, and some have similar symptoms. This makes it hard for your health care provider to know if you really have one of these diseases, and if so, which one. Getting a diagnosis can be frustrating and stressful. Often, the first symptoms are fatigue, muscle aches and a low fever. The classic sign of an autoimmune disease is inflammation, which can cause redness, heat, pain and swelling.
The diseases may also have flare-ups, when they get worse, and remissions, when symptoms get better or disappear. Treatment depends on the disease, but in most cases one important goal is to reduce inflammation. Sometimes doctors prescribe corticosteroids or other drugs that reduce your immune response.
Autoimmunity occurs when the immune system fails to recognize self antigens and mounts an immune response against the body's own cells and tissues, leading to autoimmune disease. The immune system normally develops tolerance through central and peripheral mechanisms to distinguish self from non-self. A breakdown in tolerance can result from genetic susceptibility and environmental triggers like infections that cause molecular mimicry or tissue damage releasing self antigens. Autoimmune diseases are classified as organ-specific if they target a single organ, or systemic if affecting multiple body systems.
This document provides an overview of the immune system, including both innate and adaptive immunity. It discusses the key components of the immune system such as phagocytes, lymphocytes, antibodies, the complement system, and the major histocompatibility complex. It also describes the processes of inflammation, antigen presentation, and the roles of cytokines and lymphokines. The document is intended as an introductory resource on immunology.
This document provides an overview of immune disorders and hypersensitivity reactions. It defines four types of hypersensitivity: Type I or anaphylactic hypersensitivity; Type II or cytotoxic hypersensitivity; Type III or immune complex hypersensitivity; and Type IV or cell-mediated hypersensitivity. Specific examples such as allergic rhinitis, atopic dermatitis, anaphylaxis, and serum sickness are described in detail, including their definitions, causes, pathophysiology, clinical manifestations, diagnostic assessment, and medical and nursing management. The presentation aims to help students understand immunological disorders and hypersensitivity reactions.
This document provides an overview of autoimmunity. It defines autoimmunity as the immune system attacking the body's own tissues, discusses the history of the field and how tolerance normally prevents this, and lists factors that can disrupt tolerance and lead to autoimmune disease. Some key autoimmune diseases are then described, along with criteria for diagnosing autoimmune conditions.
This document discusses immunity and autoimmunity. It begins by defining autoimmunity as the loss of tolerance to self, resulting in the production of antibodies or lymphocytes that react with self components. The key criteria for classifying a disease as autoimmune are also outlined. Several potential mechanisms for autoimmunity are then examined, including sequestered antigens, cross-reactive antigens, altered self antigens, loss of immunoregulation, and genetic factors. Finally, some examples of specific autoimmune diseases are briefly described.
This document discusses autoimmune diseases, including their mechanisms, animal models, organ-specific and systemic forms, diagnosis, and treatment approaches. It defines autoimmunity as the immune system mistakenly attacking the body's own tissues. The mechanisms discussed include molecular mimicry, failure of self-tolerance, and abnormal immune responses. Organ-specific diseases covered are Graves' disease, myasthenia gravis, IDDM, and others. Systemic diseases discussed include rheumatoid arthritis, SLE, Sjogren's syndrome, and more. Diagnosis and treatment focus on identifying autoantibodies, immunosuppressants, monoclonal antibodies, and other targeted therapies.
The document discusses autoimmunity and immunodeficiency. It defines autoimmunity as the body's immune system attacking its own antigens, potentially causing tissue damage. Normally, immune tolerance prevents this. When tolerance is breached, various autoimmune diseases can occur. The document also defines and classifies primary and secondary immunodeficiencies, providing examples of defects and common infections associated with different types of immunodeficiencies. Laboratory tests for diagnosing autoimmune diseases and immunodeficiencies are also outlined.
This document discusses autoimmune diseases from several perspectives in 3 paragraphs:
1) It provides an overview of autoimmune diseases, their causes, epidemiology, and challenges in treatment. Many diseases are difficult to cure as the immune response targets self-antigens. Genetics and the environment both contribute to disease risk.
2) It examines the role of single gene disorders in autoimmunity, highlighting specific genes like AIRE, FOXP3, and FAS that impact central and peripheral tolerance when mutated.
3) It explores the genetics and immune features of complex autoimmune diseases, which involve multiple genetic and environmental factors. Various cell types, cytokines, autoantibodies, and complement activation can drive pathogenesis
This document summarizes various immunodeficiency disorders, including both primary and secondary immunodeficiencies. It describes the main types of primary immunodeficiencies which affect phagocytic cells (18%), complement (2%), B-cells (50%), T-cells (30%) and combined defects. Specific disorders are then discussed in more detail such as chronic granulomatous disease, Chediac-Higashi syndrome, X-linked agammaglobulinemia, selective IgA deficiency, DiGeorge's syndrome, ataxia telangiectasia. Secondary immunodeficiencies can result from neoplasms, infections, decreased complement components, immunosuppressive therapies, radiation, metabolic
Chronic Salmonella typhi carrier state: a precursor to gall bladder cancer KETAN VAGHOLKAR
Typhoid fever is one of the commonest infections of the gastrointestinal tract seen in the Indian subcontinent. Association with gall stones can lead to a chronic carrier state. This is a dangerous situation as it can strongly predispose to the development of carcinoma of the gall bladder which is known to have a very poor prognosis. The pathophysiology of this carcinogenic change and its clinical implications are discussed in this paper.
The document discusses disorders of the immune system. It describes the functions of a normal immune system and what can go wrong, including immunodeficiencies where the immune system is weak or overactive. It covers specific immune disorders like allergies, autoimmune diseases, and transplant rejection. It also discusses cancer immunology and HIV/AIDS.
The document discusses the molecular mechanisms of autoimmunity, including molecular mimicry, superantigens, epitope spreading, inappropriate MHC expression, polyclonal B cell activation by viruses and bacteria, and cytokine dysregulation. It also covers genes associated with autoimmunity, environmental factors like drugs and toxins, and sex differences in autoimmune diseases.
This document provides an overview of autoimmune diseases including causes, types, links to HLA genes, treatment approaches, and mouse models. It discusses three main types of autoimmune diseases: haemolytic, localized, and systemic. Examples like Hashimoto's thyroiditis, myasthenia gravis, multiple sclerosis, type 1 diabetes, systemic lupus erythematosus, and rheumatoid arthritis are explained. The roles of HLA genes and immunosuppressive drugs in treatment are also summarized. Mouse models that replicate human autoimmune conditions are noted.
This document provides information on autoimmune disorders, including:
- Causes of autoimmunity include sequestered antigens, altered antigens, loss of immunoregulation, and loss of self-tolerance.
- Common autoimmune diseases discussed include systemic lupus erythematosus and systemic sclerosis.
- For systemic lupus erythematosus, clinical manifestations, etiology, pathology, and treatment are summarized. Oral manifestations including bleeding and ulcers are also noted.
- Systemic sclerosis causes fibrosis of the skin, subcutaneous tissue, muscles and internal organs. Its etiology is unclear but involves genetic and environmental factors.
This document discusses autoimmunity and its underlying mechanisms. Autoimmunity occurs when the immune system mistakenly attacks and destroys healthy body tissue. The immune system normally distinguishes self from non-self through mechanisms of central and peripheral tolerance that eliminate or inactivate self-reactive immune cells. A defect or breakdown in these tolerance mechanisms can lead to autoimmunity. Specific mechanisms that may cause this include exposure of normally hidden self-antigens, antigen alteration, molecular mimicry between foreign and self-antigens, emergence of forbidden self-reactive clones, and defects in regulatory T cells or other immune cells. Common autoimmune diseases are then classified as hematological, organ-specific, or systemic.
Autoimmunity occurs when the immune system loses tolerance to its own tissues and mounts an immune response against them. There are several potential mechanisms for this loss of tolerance, including molecular mimicry between foreign and self antigens, sequestered self antigens being exposed to the immune system, and failures of regulatory mechanisms that normally suppress autoreactive immune cells. Autoimmune diseases result when this autoreactivity causes tissue damage. Examples include diseases caused by autoantibodies like rheumatoid arthritis, Graves' disease, and Hashimoto's thyroiditis, as well as those caused by autoreactive T cells like multiple sclerosis and insulin-dependent diabetes.
Autoimmunity results from a failure of the immune system to distinguish self from non-self. There are several mechanisms that can cause this including genetic factors, immunological issues, and infections. Autoimmune diseases can be organ-specific, where autoantibodies attack a single organ, or non-organ specific which causes systemic damage. Common autoimmune diseases include systemic lupus erythematosus, rheumatoid arthritis, myasthenia gravis, and Sjogren's syndrome. Tissue damage in autoimmune diseases is typically caused by type II or type III hypersensitivity reactions.
This document discusses autoimmunity, including its definition as an inappropriate immune response against self cells/tissues due to self-tolerance failure. Various triggers are described, such as genetic factors like certain HLA alleles associated with diseases, environmental factors like molecular mimicry between pathogens and self-antigens, and non-genetic host factors including immunodeficiencies. Numerous autoimmune diseases are detailed along with their antibody targets and clinical features. Diagnosis involves clinical exams, labs to detect autoantibodies, and biopsies. Treatment focuses on reducing inflammation through steroids, blocking cytokines/integrins/B cells, or more extreme measures like immunosuppressants.
Autoimmunity occurs when the immune system mistakenly attacks and damages normal body tissues. There are several proposed mechanisms for how this occurs, including molecular mimicry between foreign and self-antigens. Autoimmune diseases can be organ-specific like Hashimoto's thyroiditis or systemic. Women are more susceptible than men potentially due to immune response differences, sex hormones, and genetics like two X chromosomes carrying immune genes. Treatment may involve modulating immune responses through vaccines, monoclonal antibodies, or inducing tolerance with oral antigens.
This is a powerpoint presentation on the Topic of Diseases of the immune system, part 1 - Chapter 6, based on Robbin's textbook of pathology. Prepared by Dr. Ashish Jawarkar, who is Assistant professor at Parul institute of medical sciences and research, Vadodara. Please subscribe to our youtube channel https://www.youtube.com/channel/UCwjkzK-YnJ-ra4HMOqq3Fkw . Our facebook page: facebook.com/pathologybasics. Instagram handle @pathologybasics
Your body's immune system protects you from disease and infection. But if you have an autoimmune disease, your immune system attacks healthy cells in your body by mistake. Autoimmune diseases can affect many parts of the body.
No one is sure what causes autoimmune diseases. They do tend to run in families. Women - particularly African-American, Hispanic-American, and Native-American women - have a higher risk for some autoimmune diseases.
There are more than 80 types of autoimmune diseases, and some have similar symptoms. This makes it hard for your health care provider to know if you really have one of these diseases, and if so, which one. Getting a diagnosis can be frustrating and stressful. Often, the first symptoms are fatigue, muscle aches and a low fever. The classic sign of an autoimmune disease is inflammation, which can cause redness, heat, pain and swelling.
The diseases may also have flare-ups, when they get worse, and remissions, when symptoms get better or disappear. Treatment depends on the disease, but in most cases one important goal is to reduce inflammation. Sometimes doctors prescribe corticosteroids or other drugs that reduce your immune response.
Autoimmunity occurs when the immune system fails to recognize self antigens and mounts an immune response against the body's own cells and tissues, leading to autoimmune disease. The immune system normally develops tolerance through central and peripheral mechanisms to distinguish self from non-self. A breakdown in tolerance can result from genetic susceptibility and environmental triggers like infections that cause molecular mimicry or tissue damage releasing self antigens. Autoimmune diseases are classified as organ-specific if they target a single organ, or systemic if affecting multiple body systems.
This document provides an overview of the immune system, including both innate and adaptive immunity. It discusses the key components of the immune system such as phagocytes, lymphocytes, antibodies, the complement system, and the major histocompatibility complex. It also describes the processes of inflammation, antigen presentation, and the roles of cytokines and lymphokines. The document is intended as an introductory resource on immunology.
This document provides an overview of immune disorders and hypersensitivity reactions. It defines four types of hypersensitivity: Type I or anaphylactic hypersensitivity; Type II or cytotoxic hypersensitivity; Type III or immune complex hypersensitivity; and Type IV or cell-mediated hypersensitivity. Specific examples such as allergic rhinitis, atopic dermatitis, anaphylaxis, and serum sickness are described in detail, including their definitions, causes, pathophysiology, clinical manifestations, diagnostic assessment, and medical and nursing management. The presentation aims to help students understand immunological disorders and hypersensitivity reactions.
This document provides an overview of autoimmunity. It defines autoimmunity as the immune system attacking the body's own tissues, discusses the history of the field and how tolerance normally prevents this, and lists factors that can disrupt tolerance and lead to autoimmune disease. Some key autoimmune diseases are then described, along with criteria for diagnosing autoimmune conditions.
This document discusses immunity and autoimmunity. It begins by defining autoimmunity as the loss of tolerance to self, resulting in the production of antibodies or lymphocytes that react with self components. The key criteria for classifying a disease as autoimmune are also outlined. Several potential mechanisms for autoimmunity are then examined, including sequestered antigens, cross-reactive antigens, altered self antigens, loss of immunoregulation, and genetic factors. Finally, some examples of specific autoimmune diseases are briefly described.
This document discusses autoimmune diseases, including their mechanisms, animal models, organ-specific and systemic forms, diagnosis, and treatment approaches. It defines autoimmunity as the immune system mistakenly attacking the body's own tissues. The mechanisms discussed include molecular mimicry, failure of self-tolerance, and abnormal immune responses. Organ-specific diseases covered are Graves' disease, myasthenia gravis, IDDM, and others. Systemic diseases discussed include rheumatoid arthritis, SLE, Sjogren's syndrome, and more. Diagnosis and treatment focus on identifying autoantibodies, immunosuppressants, monoclonal antibodies, and other targeted therapies.
The document discusses autoimmunity and immunodeficiency. It defines autoimmunity as the body's immune system attacking its own antigens, potentially causing tissue damage. Normally, immune tolerance prevents this. When tolerance is breached, various autoimmune diseases can occur. The document also defines and classifies primary and secondary immunodeficiencies, providing examples of defects and common infections associated with different types of immunodeficiencies. Laboratory tests for diagnosing autoimmune diseases and immunodeficiencies are also outlined.
This document discusses autoimmune diseases from several perspectives in 3 paragraphs:
1) It provides an overview of autoimmune diseases, their causes, epidemiology, and challenges in treatment. Many diseases are difficult to cure as the immune response targets self-antigens. Genetics and the environment both contribute to disease risk.
2) It examines the role of single gene disorders in autoimmunity, highlighting specific genes like AIRE, FOXP3, and FAS that impact central and peripheral tolerance when mutated.
3) It explores the genetics and immune features of complex autoimmune diseases, which involve multiple genetic and environmental factors. Various cell types, cytokines, autoantibodies, and complement activation can drive pathogenesis
This document summarizes various immunodeficiency disorders, including both primary and secondary immunodeficiencies. It describes the main types of primary immunodeficiencies which affect phagocytic cells (18%), complement (2%), B-cells (50%), T-cells (30%) and combined defects. Specific disorders are then discussed in more detail such as chronic granulomatous disease, Chediac-Higashi syndrome, X-linked agammaglobulinemia, selective IgA deficiency, DiGeorge's syndrome, ataxia telangiectasia. Secondary immunodeficiencies can result from neoplasms, infections, decreased complement components, immunosuppressive therapies, radiation, metabolic
Chronic Salmonella typhi carrier state: a precursor to gall bladder cancer KETAN VAGHOLKAR
Typhoid fever is one of the commonest infections of the gastrointestinal tract seen in the Indian subcontinent. Association with gall stones can lead to a chronic carrier state. This is a dangerous situation as it can strongly predispose to the development of carcinoma of the gall bladder which is known to have a very poor prognosis. The pathophysiology of this carcinogenic change and its clinical implications are discussed in this paper.
The document discusses Bacillus anthracis, the bacteria that causes anthrax. It causes three forms of disease - cutaneous, inhalational, and gastrointestinal. B. anthracis is an aerobic, gram-positive spore-forming bacillus. The document outlines diagnostic criteria and laboratory tests used to identify B. anthracis from clinical samples. Treatment protocols are provided for cutaneous and inhalational anthrax in both adults and children. Vaccines available for immunization against anthrax are also mentioned.
This document provides an overview of hernias and abdominal wall defects. It defines hernias as protrusions of an organ or tissue through a defect in the wall of the containing cavity. Various types of hernias are described including indirect inguinal, direct inguinal, femoral, umbilical, incisional and rare varieties. Factors that predispose to hernias as well as the anatomy, contents, coverings and complications of different hernias are discussed. Clinical features and treatment approaches are also summarized.
NECROTISING SOFT TISSUE INFECTION- Dr. Kiran Kumar G.apollobgslibrary
This document discusses necrotizing soft tissue infections (NSTI), which are characterized by rapidly progressive necrosis of subcutaneous tissue, fascia, or muscle. NSTIs are classified as fasciitis or myositis based on the affected tissue layer. The document outlines the differences between NSTI, cellulitis, and abscesses. It describes the types, presentations, risk factors, investigations, scoring systems, and treatment approaches for NSTI. Early and aggressive surgical debridement combined with broad-spectrum antibiotics is critical to reduce mortality from these severe infections.
This document describes a case of necrotizing fasciitis in a 54-year-old man. The man presented with swelling and pain in his left lower leg, along with watery discharge and skin blisters. He had a history of an insect bite a month prior. Investigation revealed elevated white blood cell count and blood sugar. The patient was diagnosed with uncontrolled diabetes and necrotizing fasciitis. He underwent fasciotomy, debridement, and skin grafting. The wound culture grew Pseudomonas aeruginosa. With aggressive treatment including antibiotics, surgery, and control of his diabetes, the patient's condition improved.
Surgical wound infection Dr Hatem El GoharyHatem Elgohary
1. Surgical wounds are at risk of infection if the protective epithelial surfaces are broken through trauma or surgery. The body has chemical, humoral, and cellular defenses against infection but these can be compromised by various risk factors.
2. Common signs of a surgical wound infection include fever, pain, pus or discharge, redness, swelling, and tenderness at the wound site. Infections are classified based on degree of contamination from clean to dirty.
3. Proper preventative measures include preoperative antibiotic prophylaxis, hygienic practices in the operating room, and careful postoperative wound management. Established infections require identification of causative organisms and targeted antibiotic treatment.
Necrotizing fasciitis is a life-threatening soft tissue infection characterized by necrosis of subcutaneous tissue and fascia. It is usually caused by bacteria entering through breaks in the skin or surgery. Clinically, it presents with severe pain and swelling spreading beyond the site of infection. Treatment requires aggressive antibiotic therapy and urgent surgical debridement of necrotic tissue to remove the infected areas. Despite treatment, complications can be severe and mortality remains high if not recognized and treated promptly.
This document discusses immunodeficiency disorders. It begins by defining immunity and the immune system. There are two types of immunodeficiency disorders: primary (congenital) and secondary (acquired). Primary disorders are inherited and cause susceptibility to infections from a young age. They are classified based on defects in humoral immunity, cell-mediated immunity, or both. Examples of specific primary disorders are provided for each category. Secondary immunodeficiency is caused by external factors like HIV/AIDS, which damages the immune system over time. The document outlines evaluation, characteristics, treatment and clinical manifestations of various primary and secondary immunodeficiencies.
This document provides an overview of immunodeficiency. It defines immunodeficiency and discusses primary and secondary immunodeficiencies. It describes the immune system and its four arms. It discusses various types of primary immunodeficiencies that affect B cells, T cells, phagocytes, and complement pathways. It also discusses common variable immunodeficiency and selective IgA deficiency. Secondary immunodeficiencies caused by AIDS, cancer, diabetes, transplantation, autoimmune diseases, steroids, asplenia, and aging are summarized. Tests for evaluating immunodeficiency and treatment options are briefly outlined.
This document discusses a case presentation of a 2-year-old boy named D. George who has been brought in by his parents due to concerns about recurrent infections. The boy has a history of frequent upper respiratory infections and ear infections, and has been hospitalized twice for infections. The document provides background on primary immunodeficiency diseases and different aspects of the immune system to help evaluate the child's condition and determine if he has an immunodeficiency.
An autoimmune disease occurs when the immune system mistakenly attacks and destroys healthy body tissue. It is caused when the immune system cannot distinguish between antigens and self tissues. Common autoimmune diseases affect tissues like blood vessels, connective tissues, endocrine glands, joints, muscles, and skin. Examples include rheumatoid arthritis and systemic lupus erythematosus. Symptoms vary depending on the disease location but often include fatigue, fever, and general illness. Diagnosis involves physical exams, blood tests, and other tests. Treatment aims to reduce symptoms, control the immune response, and maintain the ability to fight disease using immunosuppressive medications.
1. The document defines and describes different types of hernias, including their anatomy, etiology, contents, and complications.
2. Key hernia types discussed include indirect inguinal, direct inguinal, femoral, umbilical, incisional, and rare hernias like lumbar and spigelian hernias.
3. Treatment options depending on the hernia type include surgery to repair or reinforce the weak area through herniotomy, hernioplasty, or herniorrhaphy.
Immunodeficiency disorders are associated with defects or impairments in immune function that can be congenital or acquired. Primary immunodeficiency diseases involve genetic defects affecting B cell, T cell, or phagocytic cell development. Common symptoms include recurrent infections, failure to thrive, and increased susceptibility to opportunistic infections. HIV/AIDS is an acquired immunodeficiency disorder that progressively weakens the immune system by attacking CD4 cells, leaving the body vulnerable to opportunistic infections.
This document provides information about hernia surgery. It describes the different types of hernias including inguinal, incisional, femoral, umbilical, and epigastric hernias. It discusses the common presenting complaints of a hernia such as a lump or pain and precipitating factors. The document outlines the process of examining a patient for a hernia including inspection, palpation, and tests like the cough impulse and Zeimann's technique to determine the type of hernia. It also provides guidance on examining other related areas like abdominal muscles and performing a full systemic examination of the patient.
Surgical site infections - Diagnosis, treatment and Prevention guidelinesRahul Agarwal
Surgical site infections (SSIs) are among the most common and preventable hospital-acquired infections. SSIs prolong hospital stays, increase costs, and can lead to poor wound healing, pain, and even death in some cases. SSIs are defined based on the depth of infection - superficial, deep, or organ space. Risk factors include patient factors like age, diabetes, and obesity as well as operative factors like wound classification, antibiotic prophylaxis, and maintenance of sterility during surgery. Prevention focuses on preoperative patient preparation, proper intraoperative techniques, and postoperative wound management.
Hypersensitity, And Types of Hypersensitivity I, II, III, IVPervez Ali
This document discusses the four types of hypersensitivity reactions:
Type I is immediate hypersensitivity mediated by IgE antibodies. Type II involves IgG or IgM antibody-mediated cytotoxic reactions. Type III is immune complex-mediated hypersensitivity where antigen-antibody complexes activate the complement system. Type IV is cell-mediated delayed hypersensitivity that involves T lymphocytes and cytokine release. Examples of diseases involving these mechanisms include allergic rhinitis, hemolytic disease of the newborn, serum sickness, and tuberculosis.
Autoimmunity and autoimmune diseases dr. ihsan alsaimarydr.Ihsan alsaimary
Dr. ihsan edan abdulkareem alsaimary
PROFESSOR IN MEDICAL MICROBIOLOGY AND MOLECULAR IMMUNOLOGY
ihsanalsaimary@gmail.com
mobile : 009647801410838
university of basrah - college of medicine - basrah -IRAQ
Immunology Lecture day 1 ADDU section DElla Navarro
1. The document provides an overview of immunology and the immune system, including the inflammatory process, anatomy and physiology of the immune system, and different types of immune responses.
2. It discusses the immune system in detail, including the different white blood cells, lymphoid tissues, types of immunity, immune response types, stages of immune response, and immunoglobulins.
3. The document also covers primary and secondary immunodeficiencies like HIV/AIDS, and provides the stages and diagnosis of HIV infection.
The document discusses various aspects of tumor immunity and tumor antigens:
1. Tumor antigens are antigens produced by tumor cells that trigger an immune response. They can be used as tumor markers for diagnosis and potentially for cancer therapy.
2. There are two main types of tumor antigens - tumor associated antigens, which increase with tumor growth, and tumor specific transplantation antigens, which develop during tumor development and prevent tumor transplantation between identical hosts.
3. The immune system typically mounts responses against tumor antigens via antibodies and cytotoxic T cells. Understanding tumor antigens is important for cancer immunology and developing immunotherapies to treat cancer.
This document discusses autoimmune disorders, which occur when the immune system attacks the body's own cells and tissues. It provides criteria for classifying autoimmune disorders and discusses some of the potential causes, including genetic, environmental, and hormonal factors. It also summarizes some specific autoimmune diseases like rheumatoid arthritis, systemic lupus erythematosus (lupus), and provides an overview of common treatment approaches which aim to suppress the immune system and reduce inflammation.
This document discusses autoimmune diseases, including their causes, symptoms, and treatments. Some key points:
- Autoimmune diseases occur when the immune system attacks the body's own organs and tissues, causing damage. They can affect specific organs or multiple systems.
- Common autoimmune diseases include Hashimoto's thyroiditis, type 1 diabetes, Graves' disease, rheumatoid arthritis, and systemic lupus erythematosus.
- Current treatments aim to suppress the immune system response using immunosuppressive drugs, cytotoxic drugs, plasmapheresis, or organ removal. Research is also investigating ways to induce tolerance to self-antigens or remove self-reactive immune cells.
The document provides an overview of immunology topics covered in a course, including the immune system and disease, immunopathology, and therapeutic applications. The course covers basics of the immune system, innate and adaptive immunity, cells and molecules of the immune system, and applications like immunization, transplantation, and immunotherapy. Immunopathology topics include immunodeficiency, autoimmunity, hypersensitivity, and malignancies of the immune system. Therapeutic applications focus on immunization, immunomodulation, transplantation, immunosuppression, and replacement therapies.
The document defines key terms related to the immune system and its components. It describes the immune system as the body's defense against foreign invaders like bacteria, viruses, and fungi. The immune system includes white blood cells, organs like the bone marrow, lymph nodes, tonsils, thymus, and spleen. When pathogens enter the body, the immune system responds through nonspecific defenses like barriers, inflammation, and phagocytosis by white blood cells. It also has specific defenses like antibodies and lymphocytes that provide long-lasting protection against specific pathogens.
The document defines common terminology related to the immune system such as agglutination, apoptosis, complement, cytotoxic T cells, and epitope. It then summarizes the structure of the immune system including organs, cells, and functions of lymphoid and myeloid cells. Finally, it outlines the three lines of defense of the human body - anatomical/biochemical barriers, mechanical clearance by white blood cells, and the immune response through antibodies.
The document discusses the innate and adaptive immune system. It provides details on:
1) The innate immune system's first line of defense includes physical barriers like skin and membranes, inflammation, and the complement system.
2) The adaptive immune system provides another layer of protection and has B cells that secrete antibodies and T cells that help activate immune responses.
3) Autoimmune diseases occur when the immune system mistakenly attacks the body's own tissues, and examples provided are type 1 diabetes which attacks pancreatic beta cells and Myasthenia Gravis.
Immunological tolerance is a state of unresponsiveness to a particular antigen induced by prior exposure. It prevents harmful immune reactions to self-antigens. Central tolerance occurs in the thymus and bone marrow where immature cells that react to self are eliminated. Peripheral tolerance occurs when mature cells in tissues become unresponsive through deletion or lack of co-stimulation. Factors like antigen dose, route of exposure, age and genetics influence whether tolerance or immunity develops. Failure of tolerance can lead to autoimmunity where antibodies and T cells react to self-tissues, causing organ-specific or systemic diseases like rheumatoid arthritis, multiple sclerosis and diabetes.
The document discusses nursing care for children with immune disorders. It describes the immune system and how it protects the body from infection. Immune disorders can be primary (congenital) such as deficiencies in B or T lymphocytes, or secondary (acquired) from infections, medications, or other causes. Nursing focuses on preventing infection through hygiene and monitoring for symptoms. Education of families is also important so they can care for the child's special needs.
This document provides an overview of the immune system including:
1. It defines immunity and key immune system components like antigens and antibodies.
2. The immune system consists of organs like the bone marrow, thymus, lymph nodes and spleen that produce different immune cells.
3. Nonspecific immunity is the body's first line of defense against pathogens using barriers, inflammation, and other mechanisms.
4. Specific immunity responds to specific antigens using B cells and antibodies or T cells to destroy infected or abnormal cells.
5. Problems with immunity can cause issues like allergies, autoimmune diseases, and HIV/AIDS which destroys the immune system.
There are two main types of immunity: innate and adaptive. Innate immunity provides initial defense through barriers, phagocytes, and proteins. Adaptive immunity has cellular and humoral components, mediated by T and B lymphocytes, which provide stronger, antigen-specific responses. Hypersensitivity reactions are caused by immune responses against harmless antigens, and include four types. Type I is immediate and antibody-mediated. Type II involves antibody and complement attack of cells. Type III occurs when immune complexes deposit in tissues. Type IV is delayed and cell-mediated. Disorders can also result from immune deficiencies or reactions against self.
The document describes the human immune system and its defenses against pathogens. It discusses both nonspecific defenses like physical and chemical barriers provided by the skin, mucus, stomach acids, and inflammatory response, as well as specific defenses like the antibody-mediated and cell-mediated responses involving B cells, T cells, memory cells, and vaccines.
This document defines and describes different types of immunodeficiencies. It discusses primary and secondary immunodeficiencies, listing some common examples like DiGeorge's Syndrome. It then summarizes the main features of deficiencies in antibodies, T cells, neutrophils, and complement. Finally, it briefly discusses acquired immunodeficiency syndrome (AIDS) caused by HIV infection.
The document summarizes key concepts in immunology, including:
1) It defines innate and adaptive immunity, and the types of natural, acquired, active, and passive immunity.
2) It describes the cells of the immune system including B cells, T cells, macrophages, and natural killer cells.
3) It discusses antibodies, cytokines, and how the immune system can fail to distinguish self from non-self, leading to autoimmune diseases.
Autoimmunity occurs when the immune system fails to distinguish self from non-self and attacks the body's own tissues. Immune tolerance is the body's normal ability to recognize self-antigens and not mount an immune response against itself. Breakdown of tolerance can occur through immunological factors like polyclonal T cell activation, genetic factors like certain HLA antigens, and microbial infections which may trigger an autoimmune response. Autoimmune diseases are either organ-specific when autoantibodies attack a single organ, or systemic when autoantibodies affect multiple tissues throughout the body. Common autoimmune diseases include Hashimoto's thyroiditis, Graves' disease, type 1 diabetes, rheumatoid arthritis, and systemic lupus erythe
Similar to Nrsg 200 sp 2011 immunolgy hematology (20)
Co-Chairs, Val J. Lowe, MD, and Cyrus A. Raji, MD, PhD, prepared useful Practice Aids pertaining to Alzheimer’s disease for this CME/AAPA activity titled “Alzheimer’s Disease Case Conference: Gearing Up for the Expanding Role of Neuroradiology in Diagnosis and Treatment.” For the full presentation, downloadable Practice Aids, and complete CME/AAPA information, and to apply for credit, please visit us at https://bit.ly/3PvVY25. CME/AAPA credit will be available until June 28, 2025.
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
Lecture 6 -- Memory 2015.pptlearning occurs when a stimulus (unconditioned st...AyushGadhvi1
learning occurs when a stimulus (unconditioned stimulus) eliciting a response (unconditioned response) • is paired with another stimulus (conditioned stimulus)
Summer is a time for fun in the sun, but the heat and humidity can also wreak havoc on your skin. From itchy rashes to unwanted pigmentation, several skin conditions become more prevalent during these warmer months.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
How to Control Your Asthma Tips by gokuldas hospital.Gokuldas Hospital
Respiratory issues like asthma are the most sensitive issue that is affecting millions worldwide. It hampers the daily activities leaving the body tired and breathless.
The key to a good grip on asthma is proper knowledge and management strategies. Understanding the patient-specific symptoms and carving out an effective treatment likewise is the best way to keep asthma under control.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
10 Benefits an EPCR Software should Bring to EMS Organizations Traumasoft LLC
The benefits of an ePCR solution should extend to the whole EMS organization, not just certain groups of people or certain departments. It should provide more than just a form for entering and a database for storing information. It should also include a workflow of how information is communicated, used and stored across the entire organization.
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
There are two types of specific immune responses; humoral and cell mediated . Humoral immunity is mediated by B Lymphocytes that produce antibodies (IgG, IgM, IgA, IgE) and is especially important in combating acute bacterial infections. Cellular immunity is mediated by T Lymphocytes which are processed in the thymus. Cellular immunity is especially important in combating intracellular organisms such as TB, performing tumor surveillance, mediating transplant rejection, and fighting fungal and viral infections. It also mediates the delayed type hypersensitivity reaction, which underpins skin test like the one to assess for TB exposure.
The Organs of the Immune System Bone Marrow -- All the cells of the immune system are initially derived from the bone marrow through hematopoiesis. During hematopoiesis, bone marrow-derived stem cells differentiate into either mature cells of the immune system or into precursors of cells that migrate out of the bone marrow to continue their maturation elsewhere. The bone marrow produces B cells, natural killer cells, granulocytes and immature thymocytes, in addition to red blood cells and platelets. Thymus -- The function of the thymus is to produce mature T cells. Immature thymocytes leave the bone marrow and migrate into the thymus. Through maturation process sometimes referred to as thymic education, T cells that are beneficial to the immune system are spared, while those T cells that might evoke a detrimental autoimmune response are eliminated. The mature T cells are then released into the bloodstream. Spleen -- The spleen is an immunologic filter of the blood. It is made up of B cells, T cells, macrophages, dendritic cells, natural killer cells and red blood cells. In addition to capturing foreign materials (antigens) from the blood that pass through the spleen, migratory macrophages and dendritic cells bring antigens to the spleen via the bloodstream. An immune response is initiated when the macrophage or dendritic cells present the antigen to the appropriate B or T cells. This organ can be thought of as an immunological conference center. In the spleen, B cells become activated and produce large amounts of antibody. Also, old red blood cells are destroyed in the spleen. Lymph Nodes -- The lymph nodes function as an immunologic filter for the bodily fluid known as lymph. Lymph nodes are found throughout the body. Composed mostly of T cells, B cells, dendritic cells and macrophages, the nodes drain fluid from most of our tissues. Antigens are filtered out of the lymph in the lymph node before returning the lymph to the circulation. In a similar fashion as the spleen, the macrophages and dendritic cells that capture antigens present these foreign materials to T and B cells, consequently initiating an immune response.
Bone marrow produces stem cells which are undifferentiated – based on the bodies needs at the time the stem cell is maturing and the presence of specific hormones the stem cells develop into different types of mature cells – ie RBCs platelets, different types of WBCs The WBCs are the immune system cells
Our bodies first line of defense is intact skin, mucous membranes, natural flora, - lysozymes in tears, HCl in the stomach, etc When our body is invaded by a foreign body (non self) our innate (natural) or non specific immunity kicks in = immune function of the WBCs leading to inflammation – it provides initial , limited protection And our bodies 3 rd line of defense when inflammation alone can’t solve the problem is Learned or Acquired Immunity – cell mediated and antibody mediated immunity
See Chart 50-1 on page 1788
IgG = 75% of immunoglobulins. See Chart 50-2 on page 1790
The bone marrow is the source of all blood cells – including immune cells An immature undifferentiated cell is called a stem cell and it is pluripotent = multipotent = totipotent – meaning it is has multiple potentials for maturation – what type of cell it becomes is determined by the bodies needs at the time as well as the presence of cytokines = hormones that direct maturation. Erythropoietin is a cytokine made in the kidney that is necessary for erythrocyte formation WBCs are the immune system cells – in general they function to Recognize self vs non self Perform phagocytosis of foreign antigens Perform lytic destruction of antigens and unhealthy self cells Produce antibodies Perform complement activation Produce cytokines that stimulate further production of leukocytes from stem cells and stimulate leukoctye growth and activity Remember from anatomy and physiology Granulocytes = 3 phils Agranulocytes = 2 cytes : macrophages or monocytes and lymphocytes
The body has 3 types of lymphocytes – T cells, B cells, and NK cells T-Cells -- T lymphocytes are usually divided into two major subsets that are functionally and phenotypically (identifiably) different. The T helper subset, also called the CD4+ T cell, is a coordinator of immune regulation . The main function of the T helper cell is to augment or potentiate immune responses by the secretion of specialized factors that activate other white blood cells to fight off infection. Later we will earn that these are the cells that become defective in HIV. T killer/suppressor subset or CD8+ T cell. These cells are important in directly killing certain tumor cells, viral-infected cells and sometimes parasites . The CD8+ T cells are also important in down-regulation of immune responses. Both types of T cells can be found throughout the body . They often depend on the lymph nodes and spleen as sites where activation occurs, but they are also found in other tissues of the body, most notably the liver, lung, blood, and intestinal and reproductive tracts. Natural Killer Cells -- often referred to as NK cells, are similar to the killer T cell subset (CD8+ T cells). They function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. NK cells, unlike the CD8+ (killer) T cells, kill their targets without a prior "conference” in the lymphoid organs = they possess memory for past invaders and help prevent disease when similar invader is encountered again. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively. The T cells and NK cells are involved in CMI B Cells -- The major function of B lymphocytes is the production of antibodies in response to foreign proteins of bacteria, viruses, and tumor cells. Antibodies are specialized proteins that specifically recognize and bind to ONE particular protein. Antibody production and binding to a foreign substance or antigen, often is critical as a means of signaling other cells to engulf, kill or remove that substance from the body. Involved in AMI Granulocytes or Polymorphonuclear (PMN) Leukocytes -- Granulocytes are composed of three cell types identified as neutrophils, eosinophils and basophils, based on their staining characteristics with certain dyes. These cells are predominantly important in the removal of bacteria and parasites from the body. The neutrophils are the primary phagocytic cell - They engulf these foreign bodies and degrade them using their powerful enzymes. Eosinophils – parasites and allergies and Basophils signs/symptoms of inflammation. Macrophages = monocytes that have migrated from bloodstream and entered tissue – share the “vacuum cleaner – phagocytic function of neutrophils – but they live much longer. They are often referred to as scavengers or antigen-presenting cells (APC) because they pick up and ingest foreign materials and present these antigens to other T cells and B cells so that the pathogens can be recognized and killed or an antibody response can be mounted. This is one of the important first steps in the initiation of an immune response. Involved in inflammation and assist in AMI and CMI Dendritic cells are specialized antigen-presenting cells . They are found in the circulation, in peripheral tissues and in lymphoid organs. Maturing dendritic cells travel from the periphery to secondary lymphoid organs, where they present antigens to T lymphocytes.
The body has 3 types of lymphocytes – T cells, B cells, and NK cells T-Cells -- T lymphocytes are usually divided into two major subsets that are functionally and phenotypically (identifiably) different. The T helper subset, also called the CD4+ T cell, is a coordinator of immune regulation . The main function of the T helper cell is to augment or potentiate immune responses by the secretion of specialized factors that activate other white blood cells to fight off infection. Later we will earn that these are the cells that become defective in HIV. T killer/suppressor subset or CD8+ T cell. These cells are important in directly killing certain tumor cells, viral-infected cells and sometimes parasites . The CD8+ T cells are also important in down-regulation of immune responses. Both types of T cells can be found throughout the body . They often depend on the lymph nodes and spleen as sites where activation occurs, but they are also found in other tissues of the body, most notably the liver, lung, blood, and intestinal and reproductive tracts. Natural Killer Cells -- often referred to as NK cells, are similar to the killer T cell subset (CD8+ T cells). They function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. NK cells, unlike the CD8+ (killer) T cells, kill their targets without a prior "conference” in the lymphoid organs = they possess memory for past invaders and help prevent disease when similar invader is encountered again. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively. The T cells and NK cells are involved in CMI B Cells -- The major function of B lymphocytes is the production of antibodies in response to foreign proteins of bacteria, viruses, and tumor cells. Antibodies are specialized proteins that specifically recognize and bind to ONE particular protein. Antibody production and binding to a foreign substance or antigen, often is critical as a means of signaling other cells to engulf, kill or remove that substance from the body. Involved in AMI Granulocytes or Polymorphonuclear (PMN) Leukocytes -- Granulocytes are composed of three cell types identified as neutrophils, eosinophils and basophils, based on their staining characteristics with certain dyes. These cells are predominantly important in the removal of bacteria and parasites from the body. The neutrophils are the primary phagocytic cell - They engulf these foreign bodies and degrade them using their powerful enzymes. Eosinophils – parasites and allergies and Basophils signs/symptoms of inflammation. Macrophages = monocytes that have migrated from bloodstream and entered tissue – share the “vacuum cleaner – phagocytic function of neutrophils – but they live much longer. They are often referred to as scavengers or antigen-presenting cells (APC) because they pick up and ingest foreign materials and present these antigens to other T cells and B cells so that the pathogens can be recognized and killed or an antibody response can be mounted. This is one of the important first steps in the initiation of an immune response. Involved in inflammation and assist in AMI and CMI Dendritic cells are specialized antigen-presenting cells . They are found in the circulation, in peripheral tissues and in lymphoid organs. Maturing dendritic cells travel from the periphery to secondary lymphoid organs, where they present antigens to T lymphocytes.
The body has 3 types of lymphocytes – T cells, B cells, and NK cells T-Cells -- T lymphocytes are usually divided into two major subsets that are functionally and phenotypically (identifiably) different. The T helper subset, also called the CD4+ T cell, is a coordinator of immune regulation . The main function of the T helper cell is to augment or potentiate immune responses by the secretion of specialized factors that activate other white blood cells to fight off infection. Later we will earn that these are the cells that become defective in HIV. T killer/suppressor subset or CD8+ T cell. These cells are important in directly killing certain tumor cells, viral-infected cells and sometimes parasites . The CD8+ T cells are also important in down-regulation of immune responses. Both types of T cells can be found throughout the body . They often depend on the lymph nodes and spleen as sites where activation occurs, but they are also found in other tissues of the body, most notably the liver, lung, blood, and intestinal and reproductive tracts. Natural Killer Cells -- often referred to as NK cells, are similar to the killer T cell subset (CD8+ T cells). They function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. NK cells, unlike the CD8+ (killer) T cells, kill their targets without a prior "conference” in the lymphoid organs = they possess memory for past invaders and help prevent disease when similar invader is encountered again. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively. The T cells and NK cells are involved in CMI B Cells -- The major function of B lymphocytes is the production of antibodies in response to foreign proteins of bacteria, viruses, and tumor cells. Antibodies are specialized proteins that specifically recognize and bind to ONE particular protein. Antibody production and binding to a foreign substance or antigen, often is critical as a means of signaling other cells to engulf, kill or remove that substance from the body. Involved in AMI Granulocytes or Polymorphonuclear (PMN) Leukocytes -- Granulocytes are composed of three cell types identified as neutrophils, eosinophils and basophils, based on their staining characteristics with certain dyes. These cells are predominantly important in the removal of bacteria and parasites from the body. The neutrophils are the primary phagocytic cell - They engulf these foreign bodies and degrade them using their powerful enzymes. Eosinophils – parasites and allergies and Basophils signs/symptoms of inflammation. Macrophages = monocytes that have migrated from bloodstream and entered tissue – share the “vacuum cleaner – phagocytic function of neutrophils – but they live much longer. They are often referred to as scavengers or antigen-presenting cells (APC) because they pick up and ingest foreign materials and present these antigens to other T cells and B cells so that the pathogens can be recognized and killed or an antibody response can be mounted. This is one of the important first steps in the initiation of an immune response. Involved in inflammation and assist in AMI and CMI Dendritic cells are specialized antigen-presenting cells . They are found in the circulation, in peripheral tissues and in lymphoid organs. Maturing dendritic cells travel from the periphery to secondary lymphoid organs, where they present antigens to T lymphocytes.
The body has 3 types of lymphocytes – T cells, B cells, and NK cells T-Cells -- T lymphocytes are usually divided into two major subsets that are functionally and phenotypically (identifiably) different. The T helper subset, also called the CD4+ T cell, is a coordinator of immune regulation . The main function of the T helper cell is to augment or potentiate immune responses by the secretion of specialized factors that activate other white blood cells to fight off infection. Later we will earn that these are the cells that become defective in HIV. T killer/suppressor subset or CD8+ T cell. These cells are important in directly killing certain tumor cells, viral-infected cells and sometimes parasites . The CD8+ T cells are also important in down-regulation of immune responses. Both types of T cells can be found throughout the body . They often depend on the lymph nodes and spleen as sites where activation occurs, but they are also found in other tissues of the body, most notably the liver, lung, blood, and intestinal and reproductive tracts. Natural Killer Cells -- often referred to as NK cells, are similar to the killer T cell subset (CD8+ T cells). They function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. NK cells, unlike the CD8+ (killer) T cells, kill their targets without a prior "conference” in the lymphoid organs = they possess memory for past invaders and help prevent disease when similar invader is encountered again. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively. The T cells and NK cells are involved in CMI B Cells -- The major function of B lymphocytes is the production of antibodies in response to foreign proteins of bacteria, viruses, and tumor cells. Antibodies are specialized proteins that specifically recognize and bind to ONE particular protein. Antibody production and binding to a foreign substance or antigen, often is critical as a means of signaling other cells to engulf, kill or remove that substance from the body. Involved in AMI Granulocytes or Polymorphonuclear (PMN) Leukocytes -- Granulocytes are composed of three cell types identified as neutrophils, eosinophils and basophils, based on their staining characteristics with certain dyes. These cells are predominantly important in the removal of bacteria and parasites from the body. The neutrophils are the primary phagocytic cell - They engulf these foreign bodies and degrade them using their powerful enzymes. Eosinophils – parasites and allergies and Basophils signs/symptoms of inflammation. Macrophages = monocytes that have migrated from bloodstream and entered tissue – share the “vacuum cleaner – phagocytic function of neutrophils – but they live much longer. They are often referred to as scavengers or antigen-presenting cells (APC) because they pick up and ingest foreign materials and present these antigens to other T cells and B cells so that the pathogens can be recognized and killed or an antibody response can be mounted. This is one of the important first steps in the initiation of an immune response. Involved in inflammation and assist in AMI and CMI Dendritic cells are specialized antigen-presenting cells . They are found in the circulation, in peripheral tissues and in lymphoid organs. Maturing dendritic cells travel from the periphery to secondary lymphoid organs, where they present antigens to T lymphocytes.
The body has 3 types of lymphocytes – T cells, B cells, and NK cells T-Cells -- T lymphocytes are usually divided into two major subsets that are functionally and phenotypically (identifiably) different. The T helper subset, also called the CD4+ T cell, is a coordinator of immune regulation . The main function of the T helper cell is to augment or potentiate immune responses by the secretion of specialized factors that activate other white blood cells to fight off infection. Later we will earn that these are the cells that become defective in HIV. T killer/suppressor subset or CD8+ T cell. These cells are important in directly killing certain tumor cells, viral-infected cells and sometimes parasites . The CD8+ T cells are also important in down-regulation of immune responses. Both types of T cells can be found throughout the body . They often depend on the lymph nodes and spleen as sites where activation occurs, but they are also found in other tissues of the body, most notably the liver, lung, blood, and intestinal and reproductive tracts. Natural Killer Cells -- often referred to as NK cells, are similar to the killer T cell subset (CD8+ T cells). They function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. NK cells, unlike the CD8+ (killer) T cells, kill their targets without a prior "conference” in the lymphoid organs = they possess memory for past invaders and help prevent disease when similar invader is encountered again. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively. The T cells and NK cells are involved in CMI B Cells -- The major function of B lymphocytes is the production of antibodies in response to foreign proteins of bacteria, viruses, and tumor cells. Antibodies are specialized proteins that specifically recognize and bind to ONE particular protein. Antibody production and binding to a foreign substance or antigen, often is critical as a means of signaling other cells to engulf, kill or remove that substance from the body. Involved in AMI Granulocytes or Polymorphonuclear (PMN) Leukocytes -- Granulocytes are composed of three cell types identified as neutrophils, eosinophils and basophils, based on their staining characteristics with certain dyes. These cells are predominantly important in the removal of bacteria and parasites from the body. The neutrophils are the primary phagocytic cell - They engulf these foreign bodies and degrade them using their powerful enzymes. Eosinophils – parasites and allergies and Basophils signs/symptoms of inflammation. Macrophages = monocytes that have migrated from bloodstream and entered tissue – share the “vacuum cleaner – phagocytic function of neutrophils – but they live much longer. They are often referred to as scavengers or antigen-presenting cells (APC) because they pick up and ingest foreign materials and present these antigens to other T cells and B cells so that the pathogens can be recognized and killed or an antibody response can be mounted. This is one of the important first steps in the initiation of an immune response. Involved in inflammation and assist in AMI and CMI Dendritic cells are specialized antigen-presenting cells . They are found in the circulation, in peripheral tissues and in lymphoid organs. Maturing dendritic cells travel from the periphery to secondary lymphoid organs, where they present antigens to T lymphocytes.
The body has 3 types of lymphocytes – T cells, B cells, and NK cells T-Cells -- T lymphocytes are usually divided into two major subsets that are functionally and phenotypically (identifiably) different. The T helper subset, also called the CD4+ T cell, is a coordinator of immune regulation . The main function of the T helper cell is to augment or potentiate immune responses by the secretion of specialized factors that activate other white blood cells to fight off infection. Later we will earn that these are the cells that become defective in HIV. T killer/suppressor subset or CD8+ T cell. These cells are important in directly killing certain tumor cells, viral-infected cells and sometimes parasites . The CD8+ T cells are also important in down-regulation of immune responses. Both types of T cells can be found throughout the body . They often depend on the lymph nodes and spleen as sites where activation occurs, but they are also found in other tissues of the body, most notably the liver, lung, blood, and intestinal and reproductive tracts. Natural Killer Cells -- often referred to as NK cells, are similar to the killer T cell subset (CD8+ T cells). They function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. NK cells, unlike the CD8+ (killer) T cells, kill their targets without a prior "conference” in the lymphoid organs = they possess memory for past invaders and help prevent disease when similar invader is encountered again. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively. The T cells and NK cells are involved in CMI B Cells -- The major function of B lymphocytes is the production of antibodies in response to foreign proteins of bacteria, viruses, and tumor cells. Antibodies are specialized proteins that specifically recognize and bind to ONE particular protein. Antibody production and binding to a foreign substance or antigen, often is critical as a means of signaling other cells to engulf, kill or remove that substance from the body. Involved in AMI Granulocytes or Polymorphonuclear (PMN) Leukocytes -- Granulocytes are composed of three cell types identified as neutrophils, eosinophils and basophils, based on their staining characteristics with certain dyes. These cells are predominantly important in the removal of bacteria and parasites from the body. The neutrophils are the primary phagocytic cell - They engulf these foreign bodies and degrade them using their powerful enzymes. Eosinophils – parasites and allergies and Basophils signs/symptoms of inflammation. Macrophages = monocytes that have migrated from bloodstream and entered tissue – share the “vacuum cleaner – phagocytic function of neutrophils – but they live much longer. They are often referred to as scavengers or antigen-presenting cells (APC) because they pick up and ingest foreign materials and present these antigens to other T cells and B cells so that the pathogens can be recognized and killed or an antibody response can be mounted. This is one of the important first steps in the initiation of an immune response. Involved in inflammation and assist in AMI and CMI Dendritic cells are specialized antigen-presenting cells . They are found in the circulation, in peripheral tissues and in lymphoid organs. Maturing dendritic cells travel from the periphery to secondary lymphoid organs, where they present antigens to T lymphocytes.
HLAs = human leukocyte antigens There are two types of specific immune responses; humoral and cell mediated . Humoral immunity is mediated by B Lymphocytes that produce antibodies (IgG, IgM, IgA, IgE) and is especially important in combating acute bacterial infections. Cellular immunity is mediated by T Lymphocytes which are processed in the thymus. Cellular immunity is especially important in combating intracellular organisms such as TB, performing tumor surveillance, mediating transplant rejection, and fighting fungal and viral infections. It also mediates the delayed type hypersensitivity reaction, which underpins skin test like the one to assess for TB exposure. Misnomer – not just present on leukocytes – they are present on most cells What makes us unique as individuals – specify tissue type Normal part of the individual but they would act as an antigen if they entered another person’s body. The Immune cells in the body determine if an individual cell is self or non self (foreign) and takes action Humans have about 40 major HLAs that are specific antigens determined by genetics.
Without immunity we would be sick most of the time. Inflammation and immunity are the 2 major defenses that protect a person against disease/illness When the body is injured or invaded by organisms. When these defenses are working well – the individual Is said to be immunocompetent.
Self – tolerance – immune cells (WBCs) are the ONLY cells capable of determining self from non self. They accomplish this by looking at the different types of proteins present on cell membranes. Self tolerance is the special ability of WBCs to recognize healthy self cells and not attempt to attack or destroy them.
The HIV virus would be recognized by the immune system as NON SELF
See text Chap. 6, page 103
Deformities are common with RA
See Table 54-3 on page 1895. DMARDs are initiated early in tx.
Onset may be insidious and dx delayed for many years.
ANA may also be positive with RA, scleroderma TB, hepatitis, cancer; quinidine and procainamide can also cause increase in ANA