immunodeficiency
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This document discusses immunodeficiency, which is a compromised immune system that increases susceptibility to infections. It classifies immunodeficiencies by defects in T cells, B cells, phagocytes, or complement. Specific deficiencies discussed include DiGeorge syndrome, X-linked agammaglobulinemia, IgA deficiency, X-linked hyper-IgM syndrome, severe combined immunodeficiency, leukocyte defects such as chronic granulomatous disease, and complement deficiencies. Laboratory tests for diagnosis and management strategies such as immunoglobulin replacement or gene therapy are also covered.
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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.
IMMUNODEFICIENCY DISEASES
Immunodficiency or immune deficiency is the state in which immune system’s ability to fight infectious disease is compromised or entirely absent.
Immunodeficiency disorders,2010
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.
Immunodeficiency .
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.
Immunodeficiency disorders
Immunodeficiency disorders occur when the immune system is impaired or absent, resulting in increased susceptibility to infection. Primary immunodeficiencies are congenital and caused by genetic defects, while secondary immunodeficiencies are acquired through other diseases, malnutrition, or HIV infection. Clinical manifestations of primary immunodeficiencies include infectious diseases, autoimmune disorders, malignancies, anemia, thrombocytopenia, and recurrent respiratory infections. The document further categorizes immune deficiencies based on defects in B cells, T cells, or both, and describes the roles and activation of the complement system in enhancing immune responses.
B- lymphocytes
This document summarizes the key stages in B-lymphocyte maturation, generation, and activation. It discusses how B cells develop from progenitor cells in the bone marrow, where they undergo antigen-independent maturation including immunoglobulin gene rearrangement and positive and negative selection to remove self-reactive cells. Mature B cells then leave the bone marrow equipped with B cell receptors. The document also describes how B cells are activated upon binding of antigen to their receptor, requiring co-stimulation by T helper cells to initiate the antibody response.
Cell mediated & humoral immunity
Cell-mediated immunity involves T cells that recognize and eliminate intracellular pathogens. MHC class I presents endogenous antigens to activate CD8+ cytotoxic T cells to kill virally infected cells, while MHC class II presents exogenous antigens to CD4+ helper T cells to upregulate immune functions against bacteria. Humoral immunity involves B cells maturing into plasma cells upon antigen recognition, secreting antibodies, and leaving memory B cells to facilitate a faster response upon reexposure.
Secondary Immunodeficiency
Secondary Immunodeficiency
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Reference: Included in Slides
Include causes of secondary immunodeficiency including AIDS and other viral infections
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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.
IMMUNODEFICIENCY DISEASES
Immunodficiency or immune deficiency is the state in which immune system’s ability to fight infectious disease is compromised or entirely absent.
Immunodeficiency disorders,2010
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.
Immunodeficiency .
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.
Immunodeficiency disorders
Immunodeficiency disorders occur when the immune system is impaired or absent, resulting in increased susceptibility to infection. Primary immunodeficiencies are congenital and caused by genetic defects, while secondary immunodeficiencies are acquired through other diseases, malnutrition, or HIV infection. Clinical manifestations of primary immunodeficiencies include infectious diseases, autoimmune disorders, malignancies, anemia, thrombocytopenia, and recurrent respiratory infections. The document further categorizes immune deficiencies based on defects in B cells, T cells, or both, and describes the roles and activation of the complement system in enhancing immune responses.
B- lymphocytes
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Cell mediated & humoral immunity
Cell-mediated immunity involves T cells that recognize and eliminate intracellular pathogens. MHC class I presents endogenous antigens to activate CD8+ cytotoxic T cells to kill virally infected cells, while MHC class II presents exogenous antigens to CD4+ helper T cells to upregulate immune functions against bacteria. Humoral immunity involves B cells maturing into plasma cells upon antigen recognition, secreting antibodies, and leaving memory B cells to facilitate a faster response upon reexposure.
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Autoimmunity and Tolerance
The document discusses immunological tolerance and its breakdown which can lead to autoimmunity and autoimmune diseases. It explains the mechanisms of central and peripheral tolerance that normally prevent immune responses against self-antigens. Failure of these tolerance mechanisms can occur through various causes like a breakdown of T cell anergy or loss of regulatory T cells, resulting in an immune response against self-tissues and the development of autoimmune conditions.
Immunodeficiency diseases
This document provides an overview of immunodeficiency diseases. It describes how immunodeficiencies can be primary, due to abnormalities in immune system development, or secondary, resulting from other diseases or conditions. The major classifications of primary immunodeficiencies are then outlined, including humoral deficiencies affecting B cells, cellular deficiencies affecting T cells, combined deficiencies, and disorders of complement and phagocytosis. Several specific primary immunodeficiency diseases are then described in more detail. Secondary immunodeficiencies resulting from external factors like malnutrition, infection, or drugs are also briefly discussed.
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Immunologic tolerance
Central tolerance refers to deletion of self-reactive T and B cells in the thymus and bone marrow during maturation. T cells that recognize self antigens undergo apoptosis in the thymus. Peripheral tolerance uses backup mechanisms like clonal deletion through activation-induced cell death, clonal anergy from lack of co-stimulation, and suppression by regulatory T cells. These mechanisms help prevent autoimmune disease by silencing self-reactive cells that escape central tolerance.
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Primary immunodeficiency disorders involve impairments of the immune system that predispose individuals to frequent or severe infections. They can affect phagocytic cells, B lymphocytes, T lymphocytes, or the complement system. Common primary immunodeficiencies include disorders of humoral immunity, T-cell defects, and combined B- and T-cell defects. Secondary immunodeficiencies are more common and result from underlying diseases or their treatments. Medical management focuses on treating underlying conditions, identifying immunosuppressive factors, and treating infections. Nursing assessment and care includes reducing infection risks, maintaining functions, providing education and psychological support.
T CELL ACTIVATION AND IT'S TERMINATION
T cell activation requires two signals: 1) recognition of antigens displayed on antigen-presenting cells by T cell receptors and 2) co-stimulatory signals through molecules like CD28. This leads T cells to proliferate, differentiate into effector and memory cells, and perform effector functions. Proper activation requires interaction between T cells and antigen-presenting cells in lymphoid tissues, where costimulatory molecules are highly expressed. Dysregulation of T cell activation can lead to autoimmunity or susceptibility to infection.
Complement system
The document discusses the complement system, which consists of over 30 proteins produced by the liver that function in the immune system but are not antibodies. It works as a cascade system where one activation triggers another in a chain reaction. Complement activation can lead to cell lysis and generation of inflammatory substances. It plays a role in defense against bacteria and in inflammatory and autoimmune diseases. There are three complement activation pathways: classical, alternative, and lectin. The classical pathway is antibody-dependent while the alternative and lectin pathways are antibody-independent. Complement activation results in opsonization, inflammation, clearance of immune complexes, and lysis of pathogen cells.
Humoral immune response
The document summarizes the humoral immune response. It involves B cells producing antibodies that destroy extracellular microorganisms and prevent spread of intracellular infections. The process begins when a bacterium is phagocytosed by an antigen presenting cell. The antigen is processed and displayed on the cell surface. This activates helper T cells, which trigger B cell activation and antibody production. The antibodies then bind to antigens on microorganisms, marking them for destruction by immune cells and complement proteins.
Autoimmunity
The document discusses autoimmunity, which occurs when the immune system mistakenly attacks and damages normal body tissues. It begins by explaining how self-tolerance normally prevents this but can fail. Autoimmune diseases are then caused by a variety of mechanisms, including molecular mimicry between foreign and self-antigens. Both organ-specific diseases that target single organs, as well as systemic diseases with widespread effects, are described. Specific examples like Graves' disease, systemic lupus erythematosus, and rheumatoid arthritis are outlined.
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Complement system
The document summarizes the complement system. It is part of the immune system and consists of proteins that interact in a regulated cascade to eliminate pathogens and damaged cells. There are over 20 complement proteins that are activated via the classical, alternative, or lectin pathways and work in both innate and adaptive immunity. The complement system opsonizes pathogens, causes cell lysis, promotes inflammation, and clearance of immune complexes. Deficiencies or dysregulation of complements can cause diseases.
B cell Activation by T Independent & T Dependent Antigens-Dr C R Meera
During humoral immune response, Ab production is brought about by B lymphocytes. Based on the ability to induce Ab formation, antigens can be classified into T independent and T dependent antigens. Some antigens can directly induce the B cells to produce the Abs and are called T Independent Ans. However, some Ans require the help of T lymohocytes for the production of Abs from B cells. These Ans are called T Dependent Ans.
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.
B cell(Immunology)
B cells are lymphocytes that play a key role in humoral immunity by producing antibodies. B cell development occurs in the bone marrow, progressing from pro-B cells to immature B cells that express IgM, and then to mature B cells that express IgM and IgD. Activation of B cells leads to proliferation and differentiation into plasma cells in secondary lymphoid organs. Defects in B cell development or function can cause immunodeficiencies characterized by poor antibody production and recurrent bacterial infections. Some examples of B cell immunodeficiencies include X-linked agammaglobulinemia caused by mutations in BTK, IgA deficiency, and common variable immunodeficiency.
Hypersensitivity
This document provides an overview of hypersensitivity reactions. It begins with an introduction to immune responses and defines hypersensitivity as an inappropriate or exaggerated immune response that causes tissue damage. It then summarizes the four main types of hypersensitivity reactions: Type I is an immediate, IgE-mediated allergy; Type II involves antibody-mediated cell destruction; Type III occurs via immune complex deposition; and Type IV is a delayed, cell-mediated response. Each type is described in 1-2 sentences with examples given for Type I such as anaphylaxis and atopy.
Immunodeficiency ppt
This document provides information on various primary immunodeficiency disorders including common variable immunodeficiency, selective immunoglobulin deficiency, transient hypogammaglobulinemia of infancy, X-linked agammaglobulinemia, chronic mucocutaneous candidiasis, DiGeorge syndrome, X-linked lymphoproliferative syndrome, ataxia-telangiectasia, hyper-IgM syndrome, hyperimmunoglobulinemia E syndrome, severe combined immunodeficiency, and Wiskott-Aldrich syndrome. Each disorder is described in terms of its cause, symptoms, diagnosis, and treatment. Primary immunodeficiencies are hereditary disorders that impair the immune
T-lymphocytes and generation
The document discusses T lymphocytes and their generation, maturation, activation, and differentiation. It provides details on:
1) T-lymphocytes mature in the thymus gland and express T-cell receptors that recognize antigens bound to MHC molecules. They differentiate into helper T-cells, cytotoxic T-cells, memory T-cells, and regulatory T-cells.
2) T-cell receptors are composed of alpha and beta chains that undergo gene rearrangement during development.
3) T-cells mature through double negative, double positive, and single positive stages in the thymus, undergoing positive and negative selection to remove self-reactive cells.
Type i hypersensitivity ppt presentation mode
Type I hypersensitivity reactions, also known as immediate hypersensitivity reactions, are mediated by IgE antibodies. Upon re-exposure to an allergen, IgE antibodies bound to mast cells and basophils trigger the release of inflammatory mediators such as histamine. This leads to symptoms of allergy such as sneezing, itching, and potentially life-threatening anaphylaxis. Diagnosis involves skin prick tests and measuring allergen-specific IgE levels through blood tests. Repeated allergen exposure drives the sensitization process and production of more IgE antibodies in atopic individuals.
Hypersensitivity
This document discusses the four main types of hypersensitivity reactions:
Type I is an immediate reaction mediated by IgE antibodies. It causes conditions like allergic asthma.
Type II involves antibodies binding to antigens on a person's own cells, activating complement and causing cell lysis. It includes conditions like autoimmune hemolytic anemia.
Type III occurs when immune complexes are deposited in tissues, activating complement and causing inflammation and tissue damage. Examples are serum sickness and lupus nephritis.
Type IV is a delayed reaction mediated by T cells and monocytes/macrophages. It causes conditions like contact dermatitis and tuberculosis.
Autoimmunity
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.
An overview of primary immunodeficiency diseases 2014
This document provides an overview of primary immunodeficiency disorders (PIDs). It discusses the key roles of the immune system, host immune defense mechanisms including innate and acquired immunity, types of immunodeficiencies including defects in immune system components, clinical features of PIDs, accurate diagnosis and classification of PIDs, prevalence of PIDs, PID classification systems, immunopathologic basis of PID including major host defense deficiencies, primary antibody disorders, T cell/combined immunodeficiencies including severe combined immunodeficiency, and other forms of immunodeficiencies.
immunodeficeincy.pptx
Immunodeficiency diseases (IDDs) are caused by impaired immune system function and can be congenital or acquired. Congenital IDDs may result from genetic defects and can affect both adaptive and innate immunity. Severe combined immunodeficiency (SCID) is a rare, life-threatening congenital disorder where patients lack T, B, and NK cells. Acquired IDDs have secondary causes like malnutrition, radiation, medications, cancers, aging, and other chronic illnesses that weaken immune responses. Primary immunodeficiencies are classified based on which immune cells are affected.
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The document discusses immunological tolerance and its breakdown which can lead to autoimmunity and autoimmune diseases. It explains the mechanisms of central and peripheral tolerance that normally prevent immune responses against self-antigens. Failure of these tolerance mechanisms can occur through various causes like a breakdown of T cell anergy or loss of regulatory T cells, resulting in an immune response against self-tissues and the development of autoimmune conditions.
Immunodeficiency diseases
This document provides an overview of immunodeficiency diseases. It describes how immunodeficiencies can be primary, due to abnormalities in immune system development, or secondary, resulting from other diseases or conditions. The major classifications of primary immunodeficiencies are then outlined, including humoral deficiencies affecting B cells, cellular deficiencies affecting T cells, combined deficiencies, and disorders of complement and phagocytosis. Several specific primary immunodeficiency diseases are then described in more detail. Secondary immunodeficiencies resulting from external factors like malnutrition, infection, or drugs are also briefly discussed.
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Immunologic tolerance
Central tolerance refers to deletion of self-reactive T and B cells in the thymus and bone marrow during maturation. T cells that recognize self antigens undergo apoptosis in the thymus. Peripheral tolerance uses backup mechanisms like clonal deletion through activation-induced cell death, clonal anergy from lack of co-stimulation, and suppression by regulatory T cells. These mechanisms help prevent autoimmune disease by silencing self-reactive cells that escape central tolerance.
Immunodisorders primary and secondary
Primary immunodeficiency disorders involve impairments of the immune system that predispose individuals to frequent or severe infections. They can affect phagocytic cells, B lymphocytes, T lymphocytes, or the complement system. Common primary immunodeficiencies include disorders of humoral immunity, T-cell defects, and combined B- and T-cell defects. Secondary immunodeficiencies are more common and result from underlying diseases or their treatments. Medical management focuses on treating underlying conditions, identifying immunosuppressive factors, and treating infections. Nursing assessment and care includes reducing infection risks, maintaining functions, providing education and psychological support.
T CELL ACTIVATION AND IT'S TERMINATION
T cell activation requires two signals: 1) recognition of antigens displayed on antigen-presenting cells by T cell receptors and 2) co-stimulatory signals through molecules like CD28. This leads T cells to proliferate, differentiate into effector and memory cells, and perform effector functions. Proper activation requires interaction between T cells and antigen-presenting cells in lymphoid tissues, where costimulatory molecules are highly expressed. Dysregulation of T cell activation can lead to autoimmunity or susceptibility to infection.
Complement system
The document discusses the complement system, which consists of over 30 proteins produced by the liver that function in the immune system but are not antibodies. It works as a cascade system where one activation triggers another in a chain reaction. Complement activation can lead to cell lysis and generation of inflammatory substances. It plays a role in defense against bacteria and in inflammatory and autoimmune diseases. There are three complement activation pathways: classical, alternative, and lectin. The classical pathway is antibody-dependent while the alternative and lectin pathways are antibody-independent. Complement activation results in opsonization, inflammation, clearance of immune complexes, and lysis of pathogen cells.
Humoral immune response
The document summarizes the humoral immune response. It involves B cells producing antibodies that destroy extracellular microorganisms and prevent spread of intracellular infections. The process begins when a bacterium is phagocytosed by an antigen presenting cell. The antigen is processed and displayed on the cell surface. This activates helper T cells, which trigger B cell activation and antibody production. The antibodies then bind to antigens on microorganisms, marking them for destruction by immune cells and complement proteins.
Autoimmunity
The document discusses autoimmunity, which occurs when the immune system mistakenly attacks and damages normal body tissues. It begins by explaining how self-tolerance normally prevents this but can fail. Autoimmune diseases are then caused by a variety of mechanisms, including molecular mimicry between foreign and self-antigens. Both organ-specific diseases that target single organs, as well as systemic diseases with widespread effects, are described. Specific examples like Graves' disease, systemic lupus erythematosus, and rheumatoid arthritis are outlined.
Innate immunity
Immunology . classification of immunology. terminology of immunology. detail description of innate immunity. classification of innate immunity. Barrier of innate immune system, immune responses , cellular innate response receptors and signaling , PAMPS and DAMPS, Toll like receptors, Phagocytosis , cellular components of innate immunity, innate lymphoid cells, complement pathways, Mannose binding lecthin pathway, alternative pathway, inflammations, process of inflammations, fever mechanism , factor affecting innate systems, defects in innate immunity, deficiency in innate immunity, disease therapy
Complement system
The document summarizes the complement system. It is part of the immune system and consists of proteins that interact in a regulated cascade to eliminate pathogens and damaged cells. There are over 20 complement proteins that are activated via the classical, alternative, or lectin pathways and work in both innate and adaptive immunity. The complement system opsonizes pathogens, causes cell lysis, promotes inflammation, and clearance of immune complexes. Deficiencies or dysregulation of complements can cause diseases.
B cell Activation by T Independent & T Dependent Antigens-Dr C R Meera
During humoral immune response, Ab production is brought about by B lymphocytes. Based on the ability to induce Ab formation, antigens can be classified into T independent and T dependent antigens. Some antigens can directly induce the B cells to produce the Abs and are called T Independent Ans. However, some Ans require the help of T lymohocytes for the production of Abs from B cells. These Ans are called T Dependent Ans.
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.
B cell(Immunology)
B cells are lymphocytes that play a key role in humoral immunity by producing antibodies. B cell development occurs in the bone marrow, progressing from pro-B cells to immature B cells that express IgM, and then to mature B cells that express IgM and IgD. Activation of B cells leads to proliferation and differentiation into plasma cells in secondary lymphoid organs. Defects in B cell development or function can cause immunodeficiencies characterized by poor antibody production and recurrent bacterial infections. Some examples of B cell immunodeficiencies include X-linked agammaglobulinemia caused by mutations in BTK, IgA deficiency, and common variable immunodeficiency.
Hypersensitivity
This document provides an overview of hypersensitivity reactions. It begins with an introduction to immune responses and defines hypersensitivity as an inappropriate or exaggerated immune response that causes tissue damage. It then summarizes the four main types of hypersensitivity reactions: Type I is an immediate, IgE-mediated allergy; Type II involves antibody-mediated cell destruction; Type III occurs via immune complex deposition; and Type IV is a delayed, cell-mediated response. Each type is described in 1-2 sentences with examples given for Type I such as anaphylaxis and atopy.
Immunodeficiency ppt
This document provides information on various primary immunodeficiency disorders including common variable immunodeficiency, selective immunoglobulin deficiency, transient hypogammaglobulinemia of infancy, X-linked agammaglobulinemia, chronic mucocutaneous candidiasis, DiGeorge syndrome, X-linked lymphoproliferative syndrome, ataxia-telangiectasia, hyper-IgM syndrome, hyperimmunoglobulinemia E syndrome, severe combined immunodeficiency, and Wiskott-Aldrich syndrome. Each disorder is described in terms of its cause, symptoms, diagnosis, and treatment. Primary immunodeficiencies are hereditary disorders that impair the immune
T-lymphocytes and generation
The document discusses T lymphocytes and their generation, maturation, activation, and differentiation. It provides details on:
1) T-lymphocytes mature in the thymus gland and express T-cell receptors that recognize antigens bound to MHC molecules. They differentiate into helper T-cells, cytotoxic T-cells, memory T-cells, and regulatory T-cells.
2) T-cell receptors are composed of alpha and beta chains that undergo gene rearrangement during development.
3) T-cells mature through double negative, double positive, and single positive stages in the thymus, undergoing positive and negative selection to remove self-reactive cells.
Type i hypersensitivity ppt presentation mode
Type I hypersensitivity reactions, also known as immediate hypersensitivity reactions, are mediated by IgE antibodies. Upon re-exposure to an allergen, IgE antibodies bound to mast cells and basophils trigger the release of inflammatory mediators such as histamine. This leads to symptoms of allergy such as sneezing, itching, and potentially life-threatening anaphylaxis. Diagnosis involves skin prick tests and measuring allergen-specific IgE levels through blood tests. Repeated allergen exposure drives the sensitization process and production of more IgE antibodies in atopic individuals.
Hypersensitivity
This document discusses the four main types of hypersensitivity reactions:
Type I is an immediate reaction mediated by IgE antibodies. It causes conditions like allergic asthma.
Type II involves antibodies binding to antigens on a person's own cells, activating complement and causing cell lysis. It includes conditions like autoimmune hemolytic anemia.
Type III occurs when immune complexes are deposited in tissues, activating complement and causing inflammation and tissue damage. Examples are serum sickness and lupus nephritis.
Type IV is a delayed reaction mediated by T cells and monocytes/macrophages. It causes conditions like contact dermatitis and tuberculosis.
Autoimmunity
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.
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B cell Activation by T Independent & T Dependent Antigens-Dr C R Meera
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Immunodeficiency diseases (IDDs) are caused by impaired immune system function and can be congenital or acquired. Congenital IDDs may result from genetic defects and can affect both adaptive and innate immunity. Severe combined immunodeficiency (SCID) is a rare, life-threatening congenital disorder where patients lack T, B, and NK cells. Acquired IDDs have secondary causes like malnutrition, radiation, medications, cancers, aging, and other chronic illnesses that weaken immune responses. Primary immunodeficiencies are classified based on which immune cells are affected.
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- Immunodeficiencies can affect B cells, T cells, or phagocytes. Common disorders discussed are agammaglobulinemia, SCID, and chronic granulomatous disease. Management involves immunoglobulin replacement, antibiotics, stem cell transplant or gene therapy.
Primary immunodeficiency disorders
This document discusses approach to immunodeficiency disorders. It begins by explaining the four major components of the immune system that can be deficient - B cells, T cells, complement system, and phagocytes. Deficiencies can be congenital or acquired. It then describes primary immunodeficiency disorders as genetic diseases involving over 300 conditions and 150 genes. Classification systems for primary immunodeficiencies are provided based on the deficient immune component. Warning signs, characteristics, evaluation approach, diagnostic testing, and management goals for immunodeficiencies are outlined.
Immunodeficiency disorders: inherited & acquired
This presentation is an overview of primary and secondary immunodeficiency disorders with highlights on the genetic basis of primary disorders and associated factors underlying secondary disorders, as well a management of these disorders
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.
Immunodeficiency_DISORDERS.pptx.........
This document provides an overview of immunodeficiency diseases. It begins by defining immunodeficiency diseases as impairments of the body's defense mechanisms, including both specific immune functions like humoral and cell-mediated immunity as well as non-specific mechanisms. The document then distinguishes between primary immunodeficiencies, which are due to abnormalities in immune system development, and secondary immunodeficiencies caused by diseases, drugs, or other processes interfering with mature immune systems. It proceeds to describe several common primary immunodeficiency diseases categorized by deficiencies in humoral immunity, cellular immunity, or combined deficiencies. It concludes by outlining disorders of non-specific immunity including phagocyte and complement deficiencies.
Rheuma copy
The document discusses primary immunodeficiencies (PIDs), which are genetic disorders caused by defects in the immune system. It describes several key properties of the immune system and outlines deficiencies that can occur in both the innate and adaptive immune systems. Specific PIDs are then discussed in detail, including symptoms, diagnosis, and treatment options. The document emphasizes the importance of early diagnosis and molecular testing to determine the suitable treatment for each PID.
Rheuma copy
The document discusses primary immunodeficiencies (PIDs), which are genetic disorders caused by defects in the immune system. It describes several key properties of the immune system and outlines deficiencies that can occur in both the innate and adaptive immune systems. Specific PIDs are then discussed in detail, including symptoms, diagnosis, and treatment options. The document emphasizes the importance of early diagnosis and molecular testing to determine the most appropriate treatment for each PID.
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Vaccine
Vaccines provide immunity against disease by introducing an antigen to stimulate the immune system. There are two main types of immunization - passive which transfers antibodies, and active which relies on natural infection or vaccines. Vaccines work by activating the immune system's memory cells to recognize and fight pathogens. Different vaccine types include live attenuated or inactivated whole organisms, purified components, recombinant antigens, and more. Factors like incubation period and immune response determine which vaccine approach is best. Vaccines have had a major positive impact on public health by eradicating smallpox and reducing cases of diseases like measles.
Structure and function of antibody molecules
Porter first proposed the 4-chain antibody model in 1959. Antibodies, also called immunoglobulins, are Y-shaped proteins produced by B-lymphocytes in response to antigens. There are five main types of antibodies: IgG, IgA, IgM, IgD, and IgE, which are defined by their heavy chains. Each antibody consists of two light chains and two heavy chains connected by disulfide bonds. The variable region allows antibodies to bind to different antigens, while the constant region defines the antibody class. The five classes have different structures and functions, such as IgM activating the complement system as the first antibody response.
Ecological succession4
This document discusses ecological succession, which describes the process of how communities of plants and animals change over time in a particular area. There are two types of succession: primary and secondary. Primary succession occurs in areas not previously inhabited, like after a volcanic eruption, where lichens and mosses first establish, adding soil. Secondary succession takes place in previously inhabited areas affected by a disturbance like fire, where the soil remains. The final stage is a climax community, a stable ecosystem adapted to the area's conditions, until the next disturbance occurs.
Flightless bird
This document summarizes flightless birds. It begins by defining flightless birds as belonging to the superorder Palaeognathae, characterized by a Palaeognathous plate. These birds are flightless, with small heads, rudimentary wings, and well-developed legs adapted for running rather than flying. The document then discusses four orders of flightless birds - ostriches, emus, cassowaries, and kiwis. Examples are provided for each, describing their physical characteristics and habitats. In closing, the document briefly mentions penguins as another type of flightless bird found in cold southern climates.
Scope of chronobiology
Chronobiology is the study of biological rhythms with respect to time. The most important rhythm studied in chronobiology is the circadian rhythm, which occurs over approximately 24 hours. Circadian rhythms regulate many physiological processes and can be broken down into daily cycles like diurnal (day active), nocturnal (night active), and crepuscular (dawn and dusk active). The history of chronobiology dates back to the 18th century when de Mairan described circadian rhythms in plants, and Franz Halberg coined the term "circadian" in the 20th century. Biological rhythms can also occur on longer (infradian) or shorter (ultradian) time scales than 24 hours.
Immunodeficiency (1)
This document discusses immunodeficiency, including:
- It defines immunodeficiency and classifies it as either primary or secondary, specific or non-specific. Primary immunodeficiencies are inherited defects in the immune system.
- It describes common examples of primary immunodeficiencies that involve deficiencies of B cells, such as X-linked agammaglobulinemia and common variable immunodeficiency, or T cells, such as DiGeorge syndrome.
- Severe combined immunodeficiency is also discussed, which is characterized by an absence of both T and B cell immunity.
- Secondary immunodeficiencies can be caused by drugs like corticosteroids, meth
Jetlag & shift work
Jetlag is a temporary disorder caused by traveling across multiple time zones that results in the body's circadian rhythms being out of sync with the destination time. Symptoms include sleepiness, fatigue, headache, and memory loss. Both jetlag and shift work, where one works alternating day and night shifts, can disrupt biological rhythms and cause health issues like depression, sleepiness, and lack of mental alertness. To cure jetlag and shift work disorder, one should get deep sleep, do yoga, exercise, consume caffeine to stay alert during shifts, and make sure to entrain circadian rhythms through light exposure and a regular schedule.
Measures of central tendency
This document discusses different measures of central tendency, including mathematical averages, averages of position, and measures of partition values. It describes three types of mathematical averages: arithmetic mean, geometric mean, and harmonic mean. It provides the definitions and formulas for calculating each type of mean. The document also discusses two types of averages of position: median and mode. It defines median as the middlemost value when data are arranged in order, and mode as the value with the highest frequency. For each measure of central tendency, the document outlines merits and demerits. It concludes by describing relationships between the mean, median, and mode for symmetrical versus asymmetrical distributions.
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immunodeficiency
- 1. Immunodeficiency Presented by :- Sher Khan M.Sc. Ill Sem. Department of Zoology Shia P.G. College, Lucknow
- 2. Objectives • Identify that Immunodeficiency is due to a defect in the immune function. • Describe the classification of Immunodeficiency. • Explain the presentations of different types of Immuno- deficiencies (e.g. recurrent infections). • Understand the varieties of immune system deficiencies involving defects in : - T cells, B cells, phagocytes and complement. • Know the laboratory investigations for immunodeficiency disorders
- 3. Definition • A state in which the ability of the immune system to fight infectious disease is compromised or entirely absent A person who has an immunodeficiency is said to be immuno-compromised
- 7. Pattern of infections and symptoms associated with primary immunodeficiencies
- 9. - Absence or underdevelopment of the Thymus gland (hypoplasia) - Hypoparathyroidism - Facial abnormalities - Cardiovascular abnormalities A congenital defect that is marked by: DiGeorge Syndrome (Congenital Thymic Aplasia )
- 10. Children may present with tetany In the complete form: - Extreme susceptibility to viral protozoal, and fungal infections - Profound depression of T-cell numbers - Absence of T-cell responses Features of DiGeorge syndrome
- 11. Fetal thymus tissue graft (14 weeks old) Management of DiGeorge syndrome
- 13. Patients with B-cell defects are subject to: Recurrent bacterial infections but Display normal immunity to most viral and fungal infections Why ???
- 14. Diverse spectrum ranging from: - Complete absence of B-cells - Complete absence of plasma cells - Low or absent immunoglobulins - Selective absence of certain immunoglobulins - Genetic Transmission - Autosomal recessive -X-linked disease: Females : carriers (normal) Males : manifest the disease
- 15. The most common type, 80 to 90 percent Defect in Bruton Tyrosine Kinase (BTK) The defect involves a block in maturation of pre- B- cells to mature B-cells in bone marrow X-linked agammaglobulinaemia (XLA) or Bruton’s hypogammaglobulinaemia (Congenital disease)
- 16. - Reduced B-cell counts to 0.1 percent (normally 5-15 percent) - Absence of Immunoglobulins - Affected children suffer from recurrent pyogenic bacterial infections Features of XLA
- 17. IgA deficiency (1:700) Most are asymptomatic: but may have increased incidence of respiratory tract infections (R.T.I) Some have recurrent R.T.I and gastrointestinal tract symptoms Selective immunoglobulin deficiency (Congenital disease)
- 18. Characterized by: - Low IgG, IgA & IgE - Variable IgM levels most frequently high X- linked hyper-IgM Syndrome (Congenital disease)
- 19. Management of immunoglobulin deficiencies: *Periodic intravenous immunoglobulin (IVIG) reduces infectious complications
- 20. Severe Combined Immunodeficiency (SCID) (Congenital disease) Causes of SCID: Enzyme deficiencies: 1. ADA (adenosine deaminase ) deficiency 2. PNP (purine phosphorylase) deficiency Toxic metabolites accumulate in T and B cells
- 21. Features of SCID - Increased susceptibility to :viral, fungal, bacterial protozoal infections (starting at 3 months of age)
- 22. Management of SCID 1. Infusion of purified enzymes 2. Gene therapy
- 24. Congenital agranulocytosis: Defect in the gene inducing G-CSF (granulocyte colony stimulating factor) Features: Pneumonia, otitis media, abscesses Quantitative Defects
- 25. A. Defect in chemotaxis Leukocyte adhesion deficiency (LAD) Defect: in the adhesion molecules responsible of leukocyte trafficking and migration to sites of infection B. Defect in intracellular Killing Chronic granulomatous disease: Defect: in the oxidative complex responsible for producing superoxide radicals Qualitative Defects (Congenital disease)
- 26. Chronic granulomatous disease (CGD) (Congenital disease) Neutrophils lack the "respiratory burst" upon phagocytosis - Characterized by recurrent life- threatening bacterial and fungal infections and granuloma formation
- 28. Deficiency of all complement components have been described C1-C9
- 29. Laboratory diagnosis of ID 1. Complete blood count : total & differential 2. Evaluation of antibody levels and response to antigens 3. T and B cells counts (Flowcytometry) 4. Measurement of complement proteins and function (CH50) 5. Assessment of phagocytosis and respiratory burst (oxygen radicals)
- 30. Take Home Message • Immunodeficiency may be congenital or acquired • It can involve any component of the immune system such as cells, antibodies, complement etc. • Most common presentation of immunodeficiency is recurrent infections that may be fatal due to delay in diagnosis and lack of appropriate therapy