Pharm immuno19 immunodeficiency
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The document discusses primary and acquired immunodeficiencies. It describes several types of primary immunodeficiencies caused by defects in B and T lymphocyte maturation and activation. These include severe combined immunodeficiencies (SCID) caused by defects affecting lymphocyte development. The document also examines acquired immunodeficiencies, specifically describing the structure and life cycle of HIV, the stages of HIV/AIDS disease progression, and the clinical course of untreated HIV infection.
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Pharm immuno19 immunodeficiency
The document discusses primary and acquired immunodeficiencies. It describes several types of primary immunodeficiencies caused by defects in B and T lymphocyte maturation and activation. These include severe combined immunodeficiencies (SCID) caused by defects affecting lymphocyte development. Acquired immunodeficiencies discussed include HIV/AIDS, covering the virus life cycle, pathogenesis of HIV disease as it progresses to AIDS, and the clinical course from acute infection to AIDS.
Immuno1 overview
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.
Immunodeficiency
The document discusses immunodeficiency, which is a defect in the immune system that leads to failure to protect against disease. It describes primary/congenital immunodeficiency caused by genetic defects impairing immune system development or function. Secondary/acquired immunodeficiency is caused by factors like cancer treatment, burns, aging or HIV infection damaging immune cells. Specific primary immunodeficiencies discussed include combined antibody and T-cell deficiencies, T-cell deficiencies like DiGeorge Syndrome, and B-cell deficiencies like X-linked agammaglobulinemia. Defects can occur in hematopoietic stem cells, lymphoid progenitors or individual immune cell types.
Pharm immuno2 cells of the immune system
The document discusses key aspects of the immune system, including:
1) Lymphocytes like T cells, B cells, and NK cells exist with diverse antigen receptors before exposure to allow recognition of a wide range of foreign antigens.
2) Antigens trigger proliferation and differentiation of antigen-specific lymphocytes.
3) Primary lymphoid organs like the bone marrow and thymus support lymphocyte development while secondary organs like lymph nodes, spleen, and mucosa-associated lymphoid tissue induce immune responses.
Immunopathology 2
The document discusses mechanisms of transplant rejection, including cellular and antibody-mediated rejection pathways. Cellular rejection is mediated by CD8+ T cells through direct recognition of donor antigens or CD4+ T cell recognition after processing by recipient antigen presenting cells. Antibody-mediated rejection can be hyperacute via pre-existing antibodies or acute via antibodies produced after transplantation. Morphologies of rejection include hyperacute rejection within hours, acute rejection within days to months, and chronic rejection over months causing organ failure. Hematopoietic stem cell transplantation can cause graft-versus-host disease, transplant rejection, or immunodeficiency in recipients.
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Immunodeficiency 1
This document summarizes various primary immunodeficiencies, including severe combined immunodeficiencies (SCIDs) affecting both T and B lymphocytes. It also describes defects in B cell maturation, T cell development, and other lymphoid and myeloid disorders. Specific conditions discussed include SCID caused by mutations in the gamma chain gene (X-linked SCID), adenosine deaminase deficiency, and reticular dysgenesis. Defects in B cells, T cells, phagocytic cells, and combined T and B cell deficiencies are also summarized. The document provides information on the cells affected, defective functions, and inheritance patterns for many primary immunodeficiencies.
Immuno deficiency disorders
This document discusses immunodeficiency disorders. It begins by defining immunity and the immune system. There are two types of immunodeficiency disorders: primary (congenital) and secondary (acquired). Primary disorders are inherited and cause susceptibility to infections from a young age. They are classified based on defects in humoral immunity, cell-mediated immunity, or both. Examples of specific primary disorders are provided for each category. Secondary immunodeficiency is caused by external factors like HIV/AIDS, which damages the immune system over time. The document outlines evaluation, characteristics, treatment and clinical manifestations of various primary and secondary immunodeficiencies.
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Pharm immuno19 immunodeficiency
The document discusses primary and acquired immunodeficiencies. It describes several types of primary immunodeficiencies caused by defects in B and T lymphocyte maturation and activation. These include severe combined immunodeficiencies (SCID) caused by defects affecting lymphocyte development. Acquired immunodeficiencies discussed include HIV/AIDS, covering the virus life cycle, pathogenesis of HIV disease as it progresses to AIDS, and the clinical course from acute infection to AIDS.
Immuno1 overview
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.
Immunodeficiency
The document discusses immunodeficiency, which is a defect in the immune system that leads to failure to protect against disease. It describes primary/congenital immunodeficiency caused by genetic defects impairing immune system development or function. Secondary/acquired immunodeficiency is caused by factors like cancer treatment, burns, aging or HIV infection damaging immune cells. Specific primary immunodeficiencies discussed include combined antibody and T-cell deficiencies, T-cell deficiencies like DiGeorge Syndrome, and B-cell deficiencies like X-linked agammaglobulinemia. Defects can occur in hematopoietic stem cells, lymphoid progenitors or individual immune cell types.
Pharm immuno2 cells of the immune system
The document discusses key aspects of the immune system, including:
1) Lymphocytes like T cells, B cells, and NK cells exist with diverse antigen receptors before exposure to allow recognition of a wide range of foreign antigens.
2) Antigens trigger proliferation and differentiation of antigen-specific lymphocytes.
3) Primary lymphoid organs like the bone marrow and thymus support lymphocyte development while secondary organs like lymph nodes, spleen, and mucosa-associated lymphoid tissue induce immune responses.
Immunopathology 2
The document discusses mechanisms of transplant rejection, including cellular and antibody-mediated rejection pathways. Cellular rejection is mediated by CD8+ T cells through direct recognition of donor antigens or CD4+ T cell recognition after processing by recipient antigen presenting cells. Antibody-mediated rejection can be hyperacute via pre-existing antibodies or acute via antibodies produced after transplantation. Morphologies of rejection include hyperacute rejection within hours, acute rejection within days to months, and chronic rejection over months causing organ failure. Hematopoietic stem cell transplantation can cause graft-versus-host disease, transplant rejection, or immunodeficiency in recipients.
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Immunodeficiency 1
This document summarizes various primary immunodeficiencies, including severe combined immunodeficiencies (SCIDs) affecting both T and B lymphocytes. It also describes defects in B cell maturation, T cell development, and other lymphoid and myeloid disorders. Specific conditions discussed include SCID caused by mutations in the gamma chain gene (X-linked SCID), adenosine deaminase deficiency, and reticular dysgenesis. Defects in B cells, T cells, phagocytic cells, and combined T and B cell deficiencies are also summarized. The document provides information on the cells affected, defective functions, and inheritance patterns for many primary immunodeficiencies.
Immuno deficiency disorders
This document discusses immunodeficiency disorders. It begins by defining immunity and the immune system. There are two types of immunodeficiency disorders: primary (congenital) and secondary (acquired). Primary disorders are inherited and cause susceptibility to infections from a young age. They are classified based on defects in humoral immunity, cell-mediated immunity, or both. Examples of specific primary disorders are provided for each category. Secondary immunodeficiency is caused by external factors like HIV/AIDS, which damages the immune system over time. The document outlines evaluation, characteristics, treatment and clinical manifestations of various primary and secondary immunodeficiencies.
Autoimmunity
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Immunodeficiency group 3
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Inmunodeficiencia
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B - cell Deficiency
B-cell deficiency is a condition where the body has impaired humoral immunity due to a lack of proper B-cell function. B-cells play an important role in regulating the immune response, and dysregulation can lead to health issues. B-cell deficiency can be caused by not enough or non-functioning B-cells, plasma cells they differentiate into, or antibodies secreted by plasma cells. Symptoms include sinus infections, sepsis, skin infections, and pneumonia due to bacteria, fungi, viruses, and protozoa. Diagnosis involves measuring immunoglobulin levels and B-cell counts. Treatment focuses on managing infections, surveillance of potential malignancies, and immunoglobulin replacement therapy.
Immunopathology 4
This document summarizes several primary immunodeficiency disorders including:
- X-Linked Agammaglobulinemia of Bruton, caused by mutations in BTK leading to absent or low antibodies and recurrent infections. Treatment is immunoglobulin replacement.
- Common Variable Immunodeficiency, a heterogeneous group characterized by low all antibody classes. Causes recurrent infections.
- Isolated IgA Deficiency results in low mucosal immunity and infections of respiratory and gastrointestinal tracts.
- Hyper-IgM Syndrome prevents isotype switching beyond IgM production due to defects in CD40/CD40L, leading to low IgG and susceptibility to pneumonia.
It also briefly discusses Secondary immun
Immuno deficiency diseases- primary and secondary
Primary immunodeficiencies are caused by genetic defects and present early in life, while secondary immunodeficiencies are acquired through diseases, medications, malnutrition etc. and are more common. The document describes various primary immunodeficiencies including X-linked agammaglobulinemia presenting in boys after 6 months with absent antibodies, and common variable immunodeficiency presenting in adolescence with low antibodies and recurrent infections. It also discusses secondary immunodeficiencies like AIDS which is caused by HIV infection of T cells leading to severe deficiencies.
ELITE CONTROLLERS
Elite controllers of HIV infection are able to naturally control HIV through cell-mediated immunity without antiretroviral therapy. Key factors contributing to their elite status include certain HLA polymorphisms, highly functional HIV-specific CD8+ T cells, strong mucosal immunity, beneficial NK cell interactions with HLA alleles, and balanced regulatory T cell and Th17 cell responses that prevent immune activation. Their immune responses also feature polyfunctional CD8+ T cells, HIV-specific CD4+ T cell responses, and antimicrobial factors like defensins from dendritic cells that inhibit HIV at multiple stages of its life cycle.
Humoral immunity
Humoral immunity is mediated by antibodies produced by plasma cells. It involves three phases: induction, expansion/differentiation, and effector. In the induction phase, antigens react with B and T cells. In the expansion/differentiation phase, lymphocyte clones proliferate and mature. In the effector phase, antibodies exert biological effects such as neutralizing toxins, agglutinating pathogens, and complement-dependent killing. Primary responses are slow with low magnitude and IgM, while secondary responses are rapid with high magnitude and long-lived IgG.
Immunodeficiency states
This document summarizes various immunodeficiency disorders, including both primary and secondary immunodeficiencies. It describes the main types of primary immunodeficiencies which affect phagocytic cells (18%), complement (2%), B-cells (50%), T-cells (30%) and combined defects. Specific disorders are then discussed in more detail such as chronic granulomatous disease, Chediac-Higashi syndrome, X-linked agammaglobulinemia, selective IgA deficiency, DiGeorge's syndrome, ataxia telangiectasia. Secondary immunodeficiencies can result from neoplasms, infections, decreased complement components, immunosuppressive therapies, radiation, metabolic
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Primary immunodeficiencies
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B cell mediated immune response involves B cells recognizing antigens through cell surface antibodies. Upon antigen recognition, B cells become activated, proliferate, and differentiate into plasma cells that secrete large amounts of antibodies against the antigen. There are two main types of antigens involved in humoral immunity: T cell dependent antigens which require T cell help to produce high affinity antibodies and immune memory; and T cell independent antigens which can directly activate B cells to secrete antibodies without T cell involvement. The generation of high affinity antibodies and memory B cells occurs primarily in germinal centers through somatic hypermutation and affinity maturation.
Secondary Immunodeficiency
Secondary immune deficiency can result from various causes including extreme ages like newborns or the elderly, malnutrition, metabolic diseases like diabetes mellitus, surgery and trauma, and environmental conditions. The aging immune system shows declines in both innate and adaptive immunity, including fewer naive T-cells and changes in neutrophil and macrophage function. Malnutrition is also a major cause and can lead to atrophy of lymphoid organs and deficiencies in T-cells, immunoglobulins, and phagocyte function. Diseases like diabetes mellitus impair innate immunity through effects on complement function, cytokine production, and phagocytosis. Surgery and trauma disrupt barriers and cause immune dysregulation while environmental exposures such as ultraviolet light, space flight, and
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This document discusses a case presentation of a 2-year-old boy named D. George who has been brought in by his parents due to concerns about recurrent infections. The boy has a history of frequent upper respiratory infections and ear infections, and has been hospitalized twice for infections. The document provides background on primary immunodeficiency diseases and different aspects of the immune system to help evaluate the child's condition and determine if he has an immunodeficiency.
Pharm immuno3 &4 q innate immunity & complement
The document summarizes key aspects of innate immunity and the complement system. It describes how the complement system recognizes microbes via three pathways: the classical, lectin, and alternative pathways. It also outlines the three main functions of complement in host defense: opsonization, chemotaxis, and formation of the membrane attack complex. The summary concludes by mentioning how deficiencies in complement proteins can increase susceptibility to certain infections.
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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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Immunodeficiency refers to a failure of the immune system and can be either primary or secondary. Primary immunodeficiencies are caused by genetic mutations and result in diseases like X-linked agammaglobulinemia and severe combined immunodeficiency. Secondary immunodeficiencies are acquired through external factors like HIV, chemotherapy, or malnutrition. Treatment focuses on treating infections with antibiotics and boosting the immune system through vaccines or other means. Complications can vary but may include recurrent infections, autoimmune disorders, or damage to major organs.
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B - cell Deficiency
B-cell deficiency is a condition where the body has impaired humoral immunity due to a lack of proper B-cell function. B-cells play an important role in regulating the immune response, and dysregulation can lead to health issues. B-cell deficiency can be caused by not enough or non-functioning B-cells, plasma cells they differentiate into, or antibodies secreted by plasma cells. Symptoms include sinus infections, sepsis, skin infections, and pneumonia due to bacteria, fungi, viruses, and protozoa. Diagnosis involves measuring immunoglobulin levels and B-cell counts. Treatment focuses on managing infections, surveillance of potential malignancies, and immunoglobulin replacement therapy.
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This document summarizes several primary immunodeficiency disorders including:
- X-Linked Agammaglobulinemia of Bruton, caused by mutations in BTK leading to absent or low antibodies and recurrent infections. Treatment is immunoglobulin replacement.
- Common Variable Immunodeficiency, a heterogeneous group characterized by low all antibody classes. Causes recurrent infections.
- Isolated IgA Deficiency results in low mucosal immunity and infections of respiratory and gastrointestinal tracts.
- Hyper-IgM Syndrome prevents isotype switching beyond IgM production due to defects in CD40/CD40L, leading to low IgG and susceptibility to pneumonia.
It also briefly discusses Secondary immun
Immuno deficiency diseases- primary and secondary
Primary immunodeficiencies are caused by genetic defects and present early in life, while secondary immunodeficiencies are acquired through diseases, medications, malnutrition etc. and are more common. The document describes various primary immunodeficiencies including X-linked agammaglobulinemia presenting in boys after 6 months with absent antibodies, and common variable immunodeficiency presenting in adolescence with low antibodies and recurrent infections. It also discusses secondary immunodeficiencies like AIDS which is caused by HIV infection of T cells leading to severe deficiencies.
ELITE CONTROLLERS
Elite controllers of HIV infection are able to naturally control HIV through cell-mediated immunity without antiretroviral therapy. Key factors contributing to their elite status include certain HLA polymorphisms, highly functional HIV-specific CD8+ T cells, strong mucosal immunity, beneficial NK cell interactions with HLA alleles, and balanced regulatory T cell and Th17 cell responses that prevent immune activation. Their immune responses also feature polyfunctional CD8+ T cells, HIV-specific CD4+ T cell responses, and antimicrobial factors like defensins from dendritic cells that inhibit HIV at multiple stages of its life cycle.
Humoral immunity
Humoral immunity is mediated by antibodies produced by plasma cells. It involves three phases: induction, expansion/differentiation, and effector. In the induction phase, antigens react with B and T cells. In the expansion/differentiation phase, lymphocyte clones proliferate and mature. In the effector phase, antibodies exert biological effects such as neutralizing toxins, agglutinating pathogens, and complement-dependent killing. Primary responses are slow with low magnitude and IgM, while secondary responses are rapid with high magnitude and long-lived IgG.
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This document summarizes various immunodeficiency disorders, including both primary and secondary immunodeficiencies. It describes the main types of primary immunodeficiencies which affect phagocytic cells (18%), complement (2%), B-cells (50%), T-cells (30%) and combined defects. Specific disorders are then discussed in more detail such as chronic granulomatous disease, Chediac-Higashi syndrome, X-linked agammaglobulinemia, selective IgA deficiency, DiGeorge's syndrome, ataxia telangiectasia. Secondary immunodeficiencies can result from neoplasms, infections, decreased complement components, immunosuppressive therapies, radiation, metabolic
Seminar primary immunodeficiency syndrome
This document provides an overview of primary immunodeficiencies, including definitions, classifications, and details on specific deficiencies affecting B cells/antibodies, T cells, phagocytes, complement, and others. It discusses conditions like SCID, Wiskott-Aldrich syndrome, hyper-IgM syndrome, ataxia-telangiectasia, and DiGeorge syndrome. Diagnostic approaches like lymphocyte counts, genetic testing, and flow cytometry are also summarized.
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This document discusses phagocytic dysfunction and chronic granulomatous disease. It describes the different types of phagocytes, including professional phagocytes like macrophages, neutrophils, and dendritic cells. It explains the role of opsonins and receptors in phagocytosis. Chronic granulomatous disease is described as a defect in the NADPH oxidase complex resulting in impaired oxidative burst and increased susceptibility to catalase-positive bacteria. Diagnosis can be made through tests like the nitroblue tetrazolium reduction test or dihydrorhodamine flow cytometry.
Primary immunodeficiencies
Immunological Disorders can be classified into 3 distinct categories.They are Hypersensitivity, Autoimmunity and Immunodeficiency.Here in this presentation we talk about Immunodeficiency disorders.Get more on our blog : http://dentistryandmedicine.blogspot.com/
Immune Based Therapies for HIV Richard Trauger, phd
Presentation on Immune Based Therapies and their implications for HIV treatment presented at the Fenway Health Center, Boston, MA for the public education conference An End To AIDS - How A State Bill Can Change Everything conducted by SearchForACure.org, the Fenway Health
Center, and the MA Dept. of Public Health
G.2014-immuno~ (10b.humoral immunity'bcell'-jyh)2016-11-10
B cell mediated immune response involves B cells recognizing antigens through cell surface antibodies. Upon antigen recognition, B cells become activated, proliferate, and differentiate into plasma cells that secrete large amounts of antibodies against the antigen. There are two main types of antigens involved in humoral immunity: T cell dependent antigens which require T cell help to produce high affinity antibodies and immune memory; and T cell independent antigens which can directly activate B cells to secrete antibodies without T cell involvement. The generation of high affinity antibodies and memory B cells occurs primarily in germinal centers through somatic hypermutation and affinity maturation.
Secondary Immunodeficiency
Secondary immune deficiency can result from various causes including extreme ages like newborns or the elderly, malnutrition, metabolic diseases like diabetes mellitus, surgery and trauma, and environmental conditions. The aging immune system shows declines in both innate and adaptive immunity, including fewer naive T-cells and changes in neutrophil and macrophage function. Malnutrition is also a major cause and can lead to atrophy of lymphoid organs and deficiencies in T-cells, immunoglobulins, and phagocyte function. Diseases like diabetes mellitus impair innate immunity through effects on complement function, cytokine production, and phagocytosis. Surgery and trauma disrupt barriers and cause immune dysregulation while environmental exposures such as ultraviolet light, space flight, and
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Pharm immuno3 &4 q innate immunity & complement
The document summarizes key aspects of innate immunity and the complement system. It describes how the complement system recognizes microbes via three pathways: the classical, lectin, and alternative pathways. It also outlines the three main functions of complement in host defense: opsonization, chemotaxis, and formation of the membrane attack complex. The summary concludes by mentioning how deficiencies in complement proteins can increase susceptibility to certain infections.
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This document summarizes key concepts about cell-mediated immunity:
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2. Effector T cells migrate to sites of infection where they carry out functions like activating macrophages to kill intracellular pathogens.
3. CD8+ T cells recognize antigens on infected cells and kill the infected cells through release of granzymes and perforin.
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2. Cytokines secreted by lymphocytes regulate immune cell activation, growth, and differentiation. They also mediate immune-related inflammation. T helper cells activate other immune cells and help induce antibody production.
3. Cytotoxic T cells kill infected cells presenting antigens from intracellular pathogens like viruses. Natural killer cells can also kill infected or abnormal cells through both MHC-dependent and independent mechanisms.
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IMMUNODEFICIENCY DISEASES
Immunodficiency or immune deficiency is the state in which immune system’s ability to fight infectious disease is compromised or entirely absent.
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Immunodeficiency diseases are caused by defects in the immune system that result in increased susceptibility to infections. They can be primary, caused by genetic defects present from birth, or secondary and acquired from other diseases. Primary immunodeficiencies are classified according to the affected immune system component and include combined immunodeficiencies, antibody deficiencies, innate immune deficiencies, and complement deficiencies. Severe combined immunodeficiency (SCID) is fatal without treatment and results from a lack of T and B cells. Other primary immunodeficiencies include Wiskott-Aldrich syndrome and hyper IgM syndrome. Clinical manifestations include recurrent infections, autoimmune diseases, and hematolymphoid diseases.
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This document discusses immunodeficiency, including:
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- Secondary immunodeficiencies can be caused by drugs like corticosteroids, meth
Infections in immunocompromised patients
This document provides information about immunodeficiency disorders including their causes, types, clinical features, and diagnosis. It discusses primary immunodeficiencies caused by defects in the immune system components like B cells, T cells, phagocytes, and complements. It also describes secondary immunodeficiencies caused by non-immunogenic factors. Specific disorders covered include B-cell defects, T-cell deficiencies, phagocytic disorders, complement deficiencies, and acquired immunodeficiency syndrome. The modes of transmission, infectious agents, associated diseases, and structures of HIV/AIDS are detailed.
Immunodeficiency - SCID & LAD
Contents- Introduction to Immunodeficiency | Types | SCID | LAD
Immunodeficiency is the inability to produce an adequate immune response because of insufficiency or absence of antibodies, immune cells or both.
SCID & LAD are the two immunodeficiencies from primary immunodeficiency.
Ch16 (3)
This document discusses various primary immunodeficiency diseases. It notes that over 120 congenital immunodeficiency forms have been reported, affecting lymphocytes, phagocytes, and complement proteins. Specific disorders covered include Bruton's agammaglobulinemia, IgA deficiency, common variable immunodeficiency, DiGeorge anomaly, severe combined immunodeficiency, and chronic granulomatous disease. The causes, clinical manifestations, diagnostic criteria, and genetic basis are described for several of these primary immunodeficiency syndromes.
Acquired immunodeficiency syndrome.pptx
- AIDS is an acquired immunodeficiency caused by the HIV virus which affects T lymphocytes. It results in opportunistic infections and tumors due to a reduced helper T cell population. HIV is transmitted through sexual contact, blood exposure, and mother-to-child transmission.
- Laboratory diagnosis is by detecting antibodies through ELISA or detecting the virus directly through PCR, antigen detection, or viral culture. Treatment involves antiretroviral therapy using different classes of drugs targeting viral enzymes and entry.
Immunodeficiency_Huwainan.pptx
(1) Primary immunodeficiencies are caused by genetic defects that lead to blocks in the maturation or functions of the immune system. Some result in increased susceptibility to infections that can be fatal without treatment.
(2) Defects can occur in B cell, T cell, or innate immune system development. Severe combined immunodeficiency (SCID) involves defects in both B and T cells.
(3) Specific defects include X-linked SCID caused by common gamma chain mutations, autosomal SCID caused by adenosine deaminase or purine nucleoside phosphorylase deficiencies, and X-linked agammaglobulinemia caused by Bruton's ty
Pathogenisis of aids
1) HIV is a retrovirus that causes AIDS by depleting CD4 T cells, weakening the immune system.
2) HIV enters host cells via CD4 and CCR5/CXCR4 receptors, integrating its genetic material which is then transcribed and new virions are assembled and released, infecting other cells.
3) As CD4 cells are gradually depleted, the immune system weakens over time, allowing opportunistic infections and cancers to develop, eventually leading to AIDS if untreated.
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.
HIV / AIDS Pathology
The document discusses HIV and AIDS. It provides information on:
- The structure and life cycle of HIV.
- How HIV infects and destroys CD4+ T cells, leading to immunosuppression and susceptibility to opportunistic infections.
- The typical stages of untreated HIV infection from acute infection to AIDS, defined as a CD4 count below 200 or an AIDS-defining condition.
- Common opportunistic infections and cancers seen in AIDS patients due to severe immune deficiency.
COMMON VARIABLE IMMUNODEFICIENCY (CVID)
Common variable immunodeficiency (CVID) is a disorder where patients have low levels of immunoglobulins and antibodies, leading to frequent bacterial infections. It results from defects in B cells that prevent their maturation into plasma cells capable of producing antibodies. CVID is diagnosed through low immunoglobulin levels and treated with immunoglobulin replacement therapy. While the cause is unknown in most cases, it can be inherited and involves defects in B and T cell function and communication.
Defects in innate immunity
Defects in the innate immune system can compromise the body's first line of defense against microorganisms. This document outlines several such defects including those affecting leukocyte function and the complement system. Regarding leukocyte function, defects may involve leukocyte adhesion, phagolysosome fusion, microbial killing ability, or TLR signaling. Complement system deficiencies can involve components of the classical, alternative, or terminal pathways and increase susceptibility to certain bacterial or viral infections. Overall, innate immune deficiencies undermine the immune response and lead to recurrent or severe infections from pathogens like Neisseria bacteria.
ranjithakm-180315143057.pdf
This document provides an overview of immunodeficiency. It begins by defining immunodeficiency and classifying it into primary and secondary types. Primary immunodeficiency is due to genetic defects present at birth, while secondary immunodeficiency is acquired from other diseases, infections, or medications. The document further discusses specific deficiencies in B cells, T cells, complement systems, and phagocytes. It also covers severe combined immunodeficiency and common secondary causes like infections, malnutrition, and immunosuppressive drugs or therapies. Treatment options include supportive therapies with antibiotics or immunoglobulin replacement as well as definitive therapies like bone marrow transplantation or gene therapy.
Immunodeficiency
This document provides an overview of immunodeficiency. It begins by defining immunodeficiency and classifying it into primary and secondary types. Primary immunodeficiency is due to genetic defects present at birth, while secondary immunodeficiency is acquired from other diseases, infections, or medications. The document further discusses specific deficiencies in B cells, T cells, complement systems, and phagocytes. It also covers severe combined immunodeficiency and common secondary causes like infections, malnutrition, and immunosuppressive drugs or therapies. Treatment options include supportive therapies with antibiotics or immunoglobulin replacement as well as definitive therapies like bone marrow transplantation or gene therapy.
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Introduction to objective, scope and outcome the subject
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Pharm immuno19 immunodeficiency
- 1. Pharmacy-Immunology 19 Primary & Acquired Immunodeficiency Saber Hussein
- 6. Fig12-2:Congenital immunodeficiencies Fig12-2:Congenital immunodeficiencies
- 7. Features of congenital immunodeficiencies caused by defects in lymphocyte maturation Fig12-3
- 8. Features of congenital immunodeficiencies caused by defects in lymphocyte maturation Fig12-3
- 10. Congenital immunodeficiencies associated with defects in lymphocyte activation and effector functions Fig12-4: Features of some of resulting deficiency disorders
- 11. Congenital immunodeficiencies caused by defects in innate immunity Fig 12-5
- 12. Congenital immunodeficiencies caused by defects in innate immunity Fig 12-5
- 13. Acquired (secondary) immunodeficiency diseases Fig 12-6
- 14. HIV life cycle Fig 12-8 HIV life cycle
- 18. The clinical course of HIV disease Fig 12-10
Editor's Notes
- Lymphocyte maturation pathways are described in more detail in Chapter 4.
- Branchial pouches pharyngeal pouches paired evaginations of embryonic pharyngeal endoderm, between the branchial arches, extending toward the corresponding ectodermally lined branchial grooves; during development they evolve into epithelial tissues and organs, such as thymus and thyroid glands . Syn: branchial pouches, endodermal pouches Hypoplasia (h º” p ½ -pl ³“ zh … , -zh ¶ - … ) n. Incomplete or arrested development of an organ or a part
- Examples showing the sites where immune responses may be blocked are illustrated in A, and the features of some of these disorders are summarized in B