Autoimmunity - Basic Immunology
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A basic course in immunology focusing on autoimmunity and the current biologic treatments in rheumatoid arthritis
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Autoimmunity - Microbiology - Immunology - Dr.Someshwaran Rajamani December 2015
Autoimimunity - IMMUNOLOGY - SECOND MBBS STUDENTS- UNDERGRADUATE - MICROBIOLOGY MADE EASY - PPT - THEORY
Autoimmunity
1. The document discusses autoimmunity and provides objectives, definitions, classifications, and details on important autoimmune diseases like SLE and Sjogren's syndrome.
2. SLE is characterized by a vast array of autoantibodies against nuclear antigens, causing injury via immune complex deposition. It can affect multiple organs and cause nephritis, skin lesions, arthritis, and hematologic and neurological issues.
3. Sjogren's syndrome is characterized by dry eyes and mouth due to immune-mediated destruction of lacrimal and salivary glands, resulting in keratoconjunctivitis sicca and xerostomia. It is believed to be caused by an autoimmune reaction against an
Autoimmunity
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.
AUTOIMMUNITY
This document provides an overview of autoimmune diseases. It discusses how a defect in the immune system can trigger autoimmunity and lists examples of autoimmune disorders like rheumatoid arthritis, Graves' disease, and Hashimoto's thyroiditis. The causes of autoimmunity include genetic susceptibility and environmental triggers like infections. Viruses can induce autoimmunity through molecular mimicry or by damaging tissues and exposing new antigens.
Autoimmunity and autoimmune disorders
This document discusses autoimmunity and autoimmune diseases. It begins by defining autoimmunity as a breakdown of self-tolerance mechanisms that leads to an adaptive immune response against self-antigens. This can result in chronic inflammation and autoimmune disease. Several proposed mechanisms for how autoimmunity occurs are described, including defects in central and peripheral tolerance. Factors like genetics, hormones, infections, and environmental exposures are thought to contribute to loss of self-tolerance. The document then classifies and describes some examples of organ-specific and systemic autoimmune diseases in more detail.
Autoimmunity ''when good turns bad ''
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
This document discusses autoimmunity, which occurs when the immune system mistakenly attacks the body's own tissues and organs. It describes how Paul Ehrlich first proposed the concept of "horror autotoxicus" to explain this phenomenon. The mechanisms of self-tolerance that normally prevent autoimmunity can fail, leading to either organ-specific or systemic autoimmune diseases. Examples of organ-specific diseases include Hashimoto's thyroiditis, pernicious anemia, and insulin-dependent diabetes mellitus. Systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis are examples of systemic autoimmune diseases provided.
Autoimmunity and autoimmune disease
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.
Recommended
Autoimmunity - Microbiology - Immunology - Dr.Someshwaran Rajamani December 2015
Autoimimunity - IMMUNOLOGY - SECOND MBBS STUDENTS- UNDERGRADUATE - MICROBIOLOGY MADE EASY - PPT - THEORY
Autoimmunity
1. The document discusses autoimmunity and provides objectives, definitions, classifications, and details on important autoimmune diseases like SLE and Sjogren's syndrome.
2. SLE is characterized by a vast array of autoantibodies against nuclear antigens, causing injury via immune complex deposition. It can affect multiple organs and cause nephritis, skin lesions, arthritis, and hematologic and neurological issues.
3. Sjogren's syndrome is characterized by dry eyes and mouth due to immune-mediated destruction of lacrimal and salivary glands, resulting in keratoconjunctivitis sicca and xerostomia. It is believed to be caused by an autoimmune reaction against an
Autoimmunity
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.
AUTOIMMUNITY
This document provides an overview of autoimmune diseases. It discusses how a defect in the immune system can trigger autoimmunity and lists examples of autoimmune disorders like rheumatoid arthritis, Graves' disease, and Hashimoto's thyroiditis. The causes of autoimmunity include genetic susceptibility and environmental triggers like infections. Viruses can induce autoimmunity through molecular mimicry or by damaging tissues and exposing new antigens.
Autoimmunity and autoimmune disorders
This document discusses autoimmunity and autoimmune diseases. It begins by defining autoimmunity as a breakdown of self-tolerance mechanisms that leads to an adaptive immune response against self-antigens. This can result in chronic inflammation and autoimmune disease. Several proposed mechanisms for how autoimmunity occurs are described, including defects in central and peripheral tolerance. Factors like genetics, hormones, infections, and environmental exposures are thought to contribute to loss of self-tolerance. The document then classifies and describes some examples of organ-specific and systemic autoimmune diseases in more detail.
Autoimmunity ''when good turns bad ''
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
This document discusses autoimmunity, which occurs when the immune system mistakenly attacks the body's own tissues and organs. It describes how Paul Ehrlich first proposed the concept of "horror autotoxicus" to explain this phenomenon. The mechanisms of self-tolerance that normally prevent autoimmunity can fail, leading to either organ-specific or systemic autoimmune diseases. Examples of organ-specific diseases include Hashimoto's thyroiditis, pernicious anemia, and insulin-dependent diabetes mellitus. Systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis are examples of systemic autoimmune diseases provided.
Autoimmunity and autoimmune disease
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.
Mechanisms of autoimmunity
Defective tolerance or regulation of self-reactive lymphocytes is the underlying cause of all autoimmune diseases. There are four known mechanisms that can lead to this regulatory failure: negative selection of autoreactive cells in the thymus, insufficient numbers or function of regulatory T cells, defective apoptosis of mature autoreactive lymphocytes, and inadequate inhibitory signaling through receptors on lymphocytes. Genetic factors like polymorphisms in MHC and non-MHC genes interact with environmental triggers like infections and tissue damage to induce the immunological abnormalities that result in autoimmunity. Molecular mimicry and bystander activation during infections can cause cross-reactivity between foreign and self-antigens.
Autoimmunity engl
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.
AUTOIMMUNITY
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
This document discusses autoimmunity and autoimmune diseases. It begins by explaining how the immune system can mistakenly attack self-antigens, leading to autoimmunity. Several organ-specific and systemic autoimmune diseases are described in detail, including how they are mediated by direct cellular damage, stimulating or blocking autoantibodies. Current treatments aim to suppress the immune system generally but do not cure the underlying condition. Experimental therapies discussed include T-cell vaccination, peptide blockade of MHC molecules, and monoclonal antibodies.
Autoimmunity
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.
The role of infections in autoimmune disease
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.
Autoimmunity by Dr. Rakesh Prasad Sah
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
Autoimmunity is caused by a failure of self/non-self discrimination in the immune system. More than 40 human diseases are known to have an autoimmune origin, affecting 5-7% of adults, with women being affected more often than men. Left-handed individuals also seem to be more susceptible to autoimmune diseases than right-handed individuals, though the reasons for this are unclear. Common autoimmune diseases include rheumatoid arthritis, diabetes, Graves' disease, and myasthenia gravis. Potential causes of autoimmunity include the release of sequestered antigens, molecular mimicry between self and foreign antigens, genetic factors, and infections that dysregulate the immune response. Treatment options aim to suppress the immune
Autoim lecture slides
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.
Autoimmune disorders
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
Autoimmune disorders
Autoimmune diseases occur when the immune system attacks the body's own tissues and organs. There are several mechanisms that normally prevent this, including central tolerance in the thymus and bone marrow, and peripheral tolerance by regulatory T cells. A failure of these tolerance mechanisms can result in autoimmune diseases. Genetic and environmental factors also contribute to predisposing individuals. Autoimmune diseases can be organ-specific or affect multiple systems. Diagnosis involves detecting elevated levels of autoantibodies through various tests. Treatment aims to suppress immune induction and restore tolerance, as well as inhibit effector mechanisms causing organ damage.
Autoimmunity and autoimmune diseases
Autoimmune diseases occur when the immune system attacks the body's own cells and tissues. They represent a significant health burden, affecting 3-9% of the population. The immune system normally maintains tolerance to self-antigens but in autoimmunity this tolerance fails. Autoimmune diseases can be systemic, targeting ubiquitous antigens, or organ-specific, targeting particular tissues. Genetic, environmental, and hormonal factors all contribute to autoimmune disease susceptibility. Treatments aim to suppress the immune system or its inflammatory responses.
Immune system disorders
this slide contains all the basic information about the immune system disorders. The slides explains anatomy and physiology of immune system well.
Autoimmunity
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.
Autoimmune disorders
The document discusses autoimmune diseases and focuses on systemic lupus erythematosus (SLE). It describes SLE as an autoimmune disease involving multiple organs characterized by autoantibodies targeting various cells and tissues. The key mechanisms involved in SLE include genetic factors like HLA alleles, defects in immunologic tolerance, abnormal display of self antigens, and inflammation triggered by infections. The document outlines the clinical features of SLE and the spectrum of autoantibodies associated with it, with antibodies to double-stranded DNA and Smith antigen being virtually diagnostic of SLE.
Autoimmune diseases
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.
Diagnosis of autoimmune diseases
This document discusses the diagnosis of autoimmune diseases. It describes several markers that provide evidence of autoimmune diseases, such as a positive family history, presence of other autoimmune diseases, infiltrating cells in affected tissues, and improvement with immunosuppressive drugs. It also discusses several mechanisms that can lead to autoimmunity, including antigenic alteration, sequestered antigens, molecular mimicry, and polyclonal B cell activation. Common diagnostic methods are also summarized, including initial laboratory evaluation, immunological studies, and detection of autoantibodies through enzyme-linked immunosorbent assays (ELISAs).
Auto immune diseases
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.
Autoimmunity
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.
Lecture 12 immunopathology
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.
Humoral immune response
This document provides an overview of the immune response and immune system. It describes the mechanisms of innate immunity including anatomical, physiological, cellular, and inflammatory barriers that provide non-specific protection. Adaptive immunity is induced when innate immunity fails, and has antigen specificity and immunological memory. B and T lymphocytes mediate humoral and cell-mediated immunity respectively. The process of phagocytosis and antibody production are explained. Primary and secondary immune responses differ in lag period, magnitude, and antibody class. Innate and adaptive immunity cooperate to eliminate pathogens.
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Mechanisms of autoimmunity
Defective tolerance or regulation of self-reactive lymphocytes is the underlying cause of all autoimmune diseases. There are four known mechanisms that can lead to this regulatory failure: negative selection of autoreactive cells in the thymus, insufficient numbers or function of regulatory T cells, defective apoptosis of mature autoreactive lymphocytes, and inadequate inhibitory signaling through receptors on lymphocytes. Genetic factors like polymorphisms in MHC and non-MHC genes interact with environmental triggers like infections and tissue damage to induce the immunological abnormalities that result in autoimmunity. Molecular mimicry and bystander activation during infections can cause cross-reactivity between foreign and self-antigens.
Autoimmunity engl
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.
AUTOIMMUNITY
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
This document discusses autoimmunity and autoimmune diseases. It begins by explaining how the immune system can mistakenly attack self-antigens, leading to autoimmunity. Several organ-specific and systemic autoimmune diseases are described in detail, including how they are mediated by direct cellular damage, stimulating or blocking autoantibodies. Current treatments aim to suppress the immune system generally but do not cure the underlying condition. Experimental therapies discussed include T-cell vaccination, peptide blockade of MHC molecules, and monoclonal antibodies.
Autoimmunity
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.
The role of infections in autoimmune disease
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.
Autoimmunity by Dr. Rakesh Prasad Sah
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
Autoimmunity is caused by a failure of self/non-self discrimination in the immune system. More than 40 human diseases are known to have an autoimmune origin, affecting 5-7% of adults, with women being affected more often than men. Left-handed individuals also seem to be more susceptible to autoimmune diseases than right-handed individuals, though the reasons for this are unclear. Common autoimmune diseases include rheumatoid arthritis, diabetes, Graves' disease, and myasthenia gravis. Potential causes of autoimmunity include the release of sequestered antigens, molecular mimicry between self and foreign antigens, genetic factors, and infections that dysregulate the immune response. Treatment options aim to suppress the immune
Autoim lecture slides
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.
Autoimmune disorders
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
Autoimmune disorders
Autoimmune diseases occur when the immune system attacks the body's own tissues and organs. There are several mechanisms that normally prevent this, including central tolerance in the thymus and bone marrow, and peripheral tolerance by regulatory T cells. A failure of these tolerance mechanisms can result in autoimmune diseases. Genetic and environmental factors also contribute to predisposing individuals. Autoimmune diseases can be organ-specific or affect multiple systems. Diagnosis involves detecting elevated levels of autoantibodies through various tests. Treatment aims to suppress immune induction and restore tolerance, as well as inhibit effector mechanisms causing organ damage.
Autoimmunity and autoimmune diseases
Autoimmune diseases occur when the immune system attacks the body's own cells and tissues. They represent a significant health burden, affecting 3-9% of the population. The immune system normally maintains tolerance to self-antigens but in autoimmunity this tolerance fails. Autoimmune diseases can be systemic, targeting ubiquitous antigens, or organ-specific, targeting particular tissues. Genetic, environmental, and hormonal factors all contribute to autoimmune disease susceptibility. Treatments aim to suppress the immune system or its inflammatory responses.
Immune system disorders
this slide contains all the basic information about the immune system disorders. The slides explains anatomy and physiology of immune system well.
Autoimmunity
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.
Autoimmune disorders
The document discusses autoimmune diseases and focuses on systemic lupus erythematosus (SLE). It describes SLE as an autoimmune disease involving multiple organs characterized by autoantibodies targeting various cells and tissues. The key mechanisms involved in SLE include genetic factors like HLA alleles, defects in immunologic tolerance, abnormal display of self antigens, and inflammation triggered by infections. The document outlines the clinical features of SLE and the spectrum of autoantibodies associated with it, with antibodies to double-stranded DNA and Smith antigen being virtually diagnostic of SLE.
Autoimmune diseases
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.
Diagnosis of autoimmune diseases
This document discusses the diagnosis of autoimmune diseases. It describes several markers that provide evidence of autoimmune diseases, such as a positive family history, presence of other autoimmune diseases, infiltrating cells in affected tissues, and improvement with immunosuppressive drugs. It also discusses several mechanisms that can lead to autoimmunity, including antigenic alteration, sequestered antigens, molecular mimicry, and polyclonal B cell activation. Common diagnostic methods are also summarized, including initial laboratory evaluation, immunological studies, and detection of autoantibodies through enzyme-linked immunosorbent assays (ELISAs).
Auto immune diseases
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.
Autoimmunity
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.
Lecture 12 immunopathology
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.
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This document provides an overview of the immune response and immune system. It describes the mechanisms of innate immunity including anatomical, physiological, cellular, and inflammatory barriers that provide non-specific protection. Adaptive immunity is induced when innate immunity fails, and has antigen specificity and immunological memory. B and T lymphocytes mediate humoral and cell-mediated immunity respectively. The process of phagocytosis and antibody production are explained. Primary and secondary immune responses differ in lag period, magnitude, and antibody class. Innate and adaptive immunity cooperate to eliminate pathogens.
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Autoimmunity
This document discusses autoimmune diseases from several perspectives in 3 paragraphs:
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3. Autoimmunity results from a loss of self-tolerance and an immune response against self-components. It can be organ-specific or systemic. Causes of autoimmunity
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Autoimmunity - Basic Immunology
- 1. 1 Être ou ne pas être... The Immune system dilema Sam Khalil, PhD
- 3. Innate and Acquired Immunity
- 4. Vasodilatation Inflammation – Innate immunity 1 Actual Inflammatory response 2 Inflammatory mediators 2 1 3 3 Vascular permeability and dilation 4 4 Neutrophil and macrophage chemotaxis 5 6 5 Antigen Removed Phagocytosis 6 Proinflammatory cytokine release
- 7. Chronic inflammation Actual Inflammatory response Inflammatory mediators Chronic Inflammation Vascular permeability and dilation Innate Immunity Adaptive Immunity Macrophages + Lymphocytes recruited Neutrophil and macrophage chemotaxis Phagocytosis Proinflammatory cytokine release Antigen Remains
- 8. The adaptive immune system http://www.biolegend.com/pop_pathway.php?id=88
- 9. The adaptive immune system http://www.biolegend.com/pop_pathway.php?id=88
- 10. Innate Immunity Key step to antigen recognition Adaptive Immunity RECOGNIZE ONLY FOREIGN ANTIGENS
- 12. Antigenic peptide Front view Top view Side view MHC class II molecules
- 13. MHC class II molecules Not any peptide will fit in the groove but multiple possibilities per molecule (20-24 aa) Some peptide will have a better “fit” in one isotype vs the other
- 14. MHC peptide T-Lymphocytes TCR
- 15. T-cell receptor 5x1015 combinations How to select only the ones that do not react with self antigens?
- 16. Thymus 5x1015 combinations 2x107 combinations
- 17. Autoimmunity
- 19. Genetic Onset of Autoimmunity Environmental Inflammation & Bone Erosion CCP RA Timeline Birth Pre-clinical Clinical Symptoms Adult Life
- 20. Genetic Genetic Factors in RA Genetic Factors have a substantial impact on susceptibility to RA McGregor et al. Arthritis Rheum, 43:30-37 Birth
- 21. Genetic Genetic Factors in RA Strongest Associations: HLA-DRw4 alleles Birth
- 22. Genetic Antigenic Peptide Genetic Factors in RA HLA-DRw4 alleles Shared Epitope (SE) Birth Imboden J. Annu. Rev. Pathol. Mech. Dis. 2009. 4:417-434
- 23. Genetic Onset of Autoimmunity Environmental Inflammation & Bone Erosion CCP RA Timeline Birth Pre-clinical Clinical Symptoms Adult Life
- 24. BREAKTHROUGH IN RA Autoimmunity to citrullinated protein antigens has specificity for RA and identifies a clinically and genetically distinct form of RA Environmental 70% of RA patients are anti-CCP+ Environmental Factors in RA Adult Life
- 25. Environmental Environmental Factors in RA Process exist constitutively and occurs in healthy individuals. Citrullinated proteins are found in sites of inflammation including joints but are not specific to RA Adult Life However the loss of tolerance is the event specific for RA
- 26. Environmental Environmental Factors in RA Adult Life
- 27. Production of anti-CCP antibodies Genetic Environmental Citrullinated Peptide Combination of Genetic & Environmental factors HLA-DRw4 alleles Shared Epitope (SE) Birth Adult Life 27 27
- 28. Combination of Genetic & Environmental factors Annu. Rev. Immunol. 2008. 26:651–75
- 29. Genetic Onset of Autoimmunity Environmental Inflammation & Bone Erosion Observed up to 10 years before onset of disease* CCP RA Timeline + = Therefore Joint inflammation is not a requirement for the development of anti-CCP antibodies Birth Pre-clinical Clinical Symptoms Adult Life * Klareskog et al. Ann Rheum Dis 2004; 63(Suppl II): ii28-ii33
- 30. Pathologic inflammatory response ? Annu. Rev. Immunol. 2008. 26:651–75
- 31. Chronic rheumatoid arthritis Annu. Rev. Immunol. 2008. 26:651–75
- 32. Chronic inflammation Actual Inflammatory response Inflammatory mediators Chronic Inflammation Vascular permeability and dilation Innate Immunity Adaptive Immunity Macrophages + Lymphocytes recruited Neutrophil and macrophage chemotaxis Phagocytosis Proinflammatory cytokine release Antigen Remains
- 33. Pathogenesis of RA J. Clin. Invest. 118:3537–3545 (2008). doi:10.1172/JCI36389
- 34. Current Biologic agents in RA Infliximab Adalimumab Golimumab CertolizumabPegol Etanercept Ustekinumab Tocilizumab Abatacept Rituximab Infliximab Adalimumab Rituximab Adapted from Chan et al. Nature Reviews Immunology, May 2010; v10; p301-316
- 35. Current Biologic agents in RA - - - - Abatacept Rituximab Tocilizumab Anti-TNF Anakinra - - Nature Reviews Rheumatology 5, 531-541 (October 2009)
- 36. Genetic Susceptibility (HLA-DRw4) Inflammation Cytokines Pathways Citrullination of antigens in the joints Bone Erosion Environment (e.g Smoking) Immune Complexes Activation of the complement Summary Anti-CCP antibodies Insult in the joints
- 37. Genetic Susceptibility (HLA-DRw4) Inflammation Cytokines Pathways Citrullination of antigens in the joints Bone Erosion Environment (e.g Smoking) Immune Complexes Activation of the complement Summary Anti-CCP antibodies Insult in the joints ?
- 38. 38 QUESTIONS ? http://www.samkhalil.ca