Pharm immuno12 &13 tolerance & autoimmunity
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The document discusses immunologic tolerance and autoimmunity. It defines tolerance as nonresponsiveness to a self-molecule recognized by the immune system. Central and peripheral tolerance induce self-tolerance through mechanisms like clonal deletion and anergy. A breakdown in tolerance can lead to autoimmunity, where the immune system responds to self-antigens. Genetic and environmental factors can influence autoimmunity, and conditions like molecular mimicry between self and foreign antigens may trigger autoimmune responses if tolerance is breached.
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The document discusses human blood groups and the Rhesus (Rh) factor. It describes the major blood group systems, including ABO and Rh, which are most important for transfusions. The ABO system includes four blood types - A, B, AB, and O - based on the antigens on red blood cells and antibodies in plasma. The Rh system involves Rh+ and Rh- blood based on the presence or absence of Rh antigens. Incompatibility between blood groups can cause dangerous clumping of red blood cells during transfusions.
Autoimmunity
This document discusses immunological tolerance and autoimmunity. It defines central and peripheral tolerance as mechanisms by which the immune system learns to distinguish self from non-self. Central tolerance involves deletion of self-reactive lymphocytes in the thymus and bone marrow. Peripheral tolerance mechanisms include clonal deletion, anergy, and suppression. Failure of tolerance can lead to autoimmune diseases, which are influenced by genetic, hormonal, and environmental factors. Common triggers include molecular mimicry between microbial and self-antigens.
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.
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.
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
Tolerance & autoimmunity
1. Immune tolerance occurs when the immune system fails to respond to an antigen it has previously been exposed to, resulting in non-reactivity to that antigen. Tolerance is important for avoiding autoimmune reactions to self-antigens.
2. Tolerance can occur through several mechanisms, including clonal deletion of autoreactive T and B cells in the thymus and bone marrow, clonal anergy of autoreactive cells, ignorance of sequestered self-antigens, and receptor editing of B cells.
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
Hypersensitivity, Tolerance and autoimmunity
This document discusses different types of hypersensitivity reactions and autoimmune diseases. It covers four types of hypersensitivity reactions: type I involves IgE antibodies and mast cells/basophils; type II involves IgG/IgM antibodies activating complement and lysing cells; type III involves immune complex formation and deposition; type IV involves delayed T cell responses. Examples and mechanisms of each type are provided. The document also discusses tolerance, genetic and environmental factors in autoimmunity, common autoimmune diseases and the antibodies associated with them.
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The document provides an overview of the immune system, including:
1. It differentiates between innate and adaptive immunity and describes cells involved in each.
2. It outlines the properties of adaptive immunity including specificity and memory.
3. It describes the tissues and organs of the immune system including peripheral lymphoid organs and lymphocyte circulation.
Tolerance and AD 23.pdf
1. The document discusses mechanisms of central and peripheral tolerance that prevent autoimmune diseases. Central tolerance involves positive and negative selection in the thymus to eliminate self-reactive T cells, aided by the AIRE gene.
2. Peripheral tolerance mechanisms help control self-reactive T cells that escape thymic selection. These include clonal deletion, anergy, and regulation by Treg cells. Anergy involves a lack of response upon re-exposure to self-antigen.
3. Tolerance is important physiologically for organ transplants, maternal-fetal tolerance, and tolerance of commensal gut microbes. A breakdown in tolerance can lead to autoimmune diseases.
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.
Immunological tolerance and mechanisms involved
Immunological tolerance is the unresponsiveness of the immune system to antigens that have been encountered before. Tolerance to self-antigens, called self-tolerance, is important so the immune system does not attack the body's own tissues. Self-tolerance is achieved through central tolerance in the thymus and peripheral tolerance in mature lymphocytes. Central tolerance eliminates self-reactive T cells, while peripheral tolerance uses regulatory T cells, cytokines like IL-10 and TGF-β, and apoptosis to control self-reactive cells that escape central tolerance.
Basic Features of Autoimmune Diseases
This document provides an overview of autoimmune diseases and immunologic tolerance. It discusses several key points:
- Autoimmune diseases result from immune reactions against self antigens and can affect connective tissues/blood vessels.
- Normal tolerance to self antigens occurs through central tolerance in the thymus and bone marrow and peripheral tolerance in tissues.
- Breakdown of tolerance and autoimmunity are caused by genetic susceptibility and environmental triggers that alter self antigen display/responses.
- Many autoimmune diseases are associated with specific HLA alleles, though they generally have complex, multigenic inheritance.
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.
Immunological tolerance
Central and peripheral tolerance mechanisms exist to prevent immune responses against self-antigens. Central tolerance occurs in the thymus through clonal deletion of self-reactive T cells. Peripheral tolerance can occur through clonal anergy, where T cells are not activated due to lack of co-stimulation, or clonal ignorance, where self-reactive T cells do not encounter self-antigens. B cell tolerance occurs through clonal deletion in the bone marrow or clonal anergy in the periphery.
Immunotolerance: mechanism and consequence
The document discusses several key mechanisms by which the immune system maintains tolerance to self-antigens to avoid autoimmunity. These include central tolerance in the thymus through negative selection which deletes self-reactive T cells, peripheral tolerance through ignorance, anergy, suppression and regulatory T cells, and the concept that tolerance is the default response unless danger signals are present to trigger an immune response. The timing of antigen exposure is also important, as antigens encountered during early development are more likely to induce tolerance.
Tolerance and autoimmunity
An undergraduate lecture on immunologic tolerance, it's various types and how a breakdown of tolerance contributes to the pathogenesis of autoimmune diseases. Additionally a small quiz at the end to gauge the students' learning.
IMMUNOLOGICAL TOLERANCE AND MODULATION PPT
This document discusses immunological tolerance and immunomodulation. It defines tolerance as the mechanism by which the immune system does not react to self-antigens. Central tolerance occurs in the thymus and bone marrow through mechanisms like clonal deletion and receptor editing to remove self-reactive T and B cells. Peripheral tolerance uses mechanisms like clonal anergy and regulatory T cells to prevent responses to self-antigens. Immunomodulation involves substances that suppress or stimulate immune responses through various mechanisms. Common immunosuppressants discussed include glucocorticoids, cyclosporine, and antiproliferative drugs which are used for organ transplants and autoimmune diseases.
Autoimmunity, definition , Autoimmune disorders dorders
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
Immune tolerance CORRECTED.pptx
This document defines immune tolerance and describes its three main forms: central tolerance, peripheral tolerance, and self-tolerance. Central tolerance occurs as T cells develop in the thymus, where self-reactive cells are deleted. Peripheral tolerance maintains tolerance throughout the body via mechanisms like lack of costimulation and regulatory T cells. Self-tolerance is the normal lack of an immune response to self-antigens, and its breakdown can lead to autoimmune diseases.
Adaptive immunity
The document summarizes key principles of the adaptive immune response. It describes how adaptive immunity arose due to limitations of innate immunity, including lack of specificity and memory. The adaptive response involves T and B lymphocytes that recognize specific antigens through cell surface receptors. Activation of T and B cells requires recognition of antigen along with costimulatory signals. This leads to clonal expansion and generation of effector cells and immunological memory. Adaptive immunity allows for tailored, amplified responses with self/non-self discrimination and immunological memory.
No 13 immunological_tolerance
The document discusses the history and mechanisms of immunological tolerance. It describes how Owen first observed that sharing a blood system in utero led to tolerance between non-identical twins. Burnet then postulated that there is a window during immune system immaturity where antigens can induce tolerance. Medawar found lifelong tolerance could be induced by transferring cells in early life but not later. The document also discusses the "danger hypothesis" and controlled cell death in preventing autoimmunity.
Autoimmunity dwd lect
This document discusses autoimmunity and provides examples of autoimmune diseases to illustrate the mechanisms. It defines autoimmunity as the condition where the immune system attacks self-antigens, potentially causing damage. Several mechanisms normally maintain tolerance to self-antigens, but breakdowns can lead to autoimmune diseases. Examples provided include Hashimoto's thyroiditis, systemic lupus erythematosus, rheumatoid arthritis, and others. Diagnostic tests for some diseases like SLE are also summarized.
Principles of tolerance and autoimmune diseases
This document discusses principles of immunological tolerance and autoimmunity. It describes how central tolerance in the thymus and bone marrow eliminates self-reactive immune cells, while peripheral tolerance mechanisms like T cell anergy, activation-induced cell death, and regulatory T cells control immune responses in tissues. Failure of these tolerance mechanisms can lead to autoimmunity when immune cells attack the body's own tissues and organs. Certain genetic factors like HLA alleles are also associated with increased risk of autoimmune diseases. The roles of infection in potentially triggering autoimmunity through molecular mimicry are also mentioned.
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.
Immunity&hypersestivity
This document discusses immunity and hypersensitivity. It defines key terms like allergen, allergy, allogeneic, allograft, atopy, and more. It also describes different immune cells like B lymphocytes, T lymphocytes, macrophages, and their roles. It discusses the major histocompatibility complex and its importance in transplantation and regulating immunity. Finally, it covers different diseases of immunity like immunodeficiencies, hypersensitivity reactions, autoimmune diseases, and acquired immunodeficiency syndrome (AIDS).
Immune tolerance
Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism. Immune tolerance is important for normal physiology. Central tolerance is the main way the immune system learns to discriminate self from non-self. Peripheral tolerance is key to preventing over-reactivity of the immune system to various environmental entities (allergens, gut microbes, etc.).
Adaptive Immunity Chapter 17 Tortora
The document summarizes adaptive immunity and the immune system. It describes the two types of adaptive immunity - active and passive, which can be acquired naturally or artificially. It also details the roles of B cells and T cells in humoral and cell-mediated immunity, including antibody production, antigen recognition, and immune memory. Hypersensitivities are immune reactions beyond normal responses, classified into four types based on mechanisms.
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