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    DR - Tjok. Istri Anom Saturti, Sppd. Mars

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    Yogiswara Karang
    1. Hypersensitivity reactions are excessive or aberrant immune responses that can manifest as immediate hypersensitivity (Type I), antibody-mediated hypersensitivity (Type II), immune complex-mediated hypersensitivity (Type III), or cell-mediated hypersensitivity (Type IV). 2. Type I hypersensitivity is IgE-mediated and involves mast cell degranulation, while Type IV is a delayed-type hypersensitivity mediated by T cells. 3. These hypersensitivity reactions can cause a variety of diseases through different pathogenic immune mechanisms and result in tissue damage, such as vasodilation and edema in Type I reactions or cellular infiltration and granuloma formation in Type IV.

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    DR - Tjok. Istri Anom Saturti, Sppd. Mars

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    Yogiswara Karang
    26 views16 pages
    1. Hypersensitivity reactions are excessive or aberrant immune responses that can manifest as immediate hypersensitivity (Type I), antibody-mediated hypersensitivity (Type II), immune complex-mediated hypersensitivity (Type III), or cell-mediated hypersensitivity (Type IV). 2. Type I hypersensitivity is IgE-mediated and involves mast cell degranulation, while Type IV is a delayed-type hypersensitivity mediated by T cells. 3. These hypersensitivity reactions can cause a variety of diseases through different pathogenic immune mechanisms and result in tissue damage, such as vasodilation and edema in Type I reactions or cellular infiltration and granuloma formation in Type IV.

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    LECTURE 14 Comprehend Hypersensitivity

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    1. Hypersensitivity reactions are excessive or aberrant immune responses that can manifest as immediate hypersensitivity (Type I), antibody-mediated hypersensitivity (Type II), immune complex-mediated hypersensitivity (Type III), or cell-mediated hypersensitivity (Type IV). 2. Type I hypersensitivity is IgE-mediated and involves mast cell degranulation, while Type IV is a delayed-type hypersensitivity mediated by T cells. 3. These hypersensitivity reactions can cause a variety of diseases through different pathogenic immune mechanisms and result in tissue damage, such as vasodilation and edema in Type I reactions or cellular infiltration and granuloma formation in Type IV.

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    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    26 views16 pages

    DR - Tjok. Istri Anom Saturti, Sppd. Mars

    Uploaded by

    Yogiswara Karang
    1. Hypersensitivity reactions are excessive or aberrant immune responses that can manifest as immediate hypersensitivity (Type I), antibody-mediated hypersensitivity (Type II), immune complex-mediated hypersensitivity (Type III), or cell-mediated hypersensitivity (Type IV). 2. Type I hypersensitivity is IgE-mediated and involves mast cell degranulation, while Type IV is a delayed-type hypersensitivity mediated by T cells. 3. These hypersensitivity reactions can cause a variety of diseases through different pathogenic immune mechanisms and result in tissue damage, such as vasodilation and edema in Type I reactions or cellular infiltration and granuloma formation in Type IV.

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    of 16

    dr.Tjok. Istri Anom Saturti,SpPD.

    MARS

    Div of Allergy Immunology , Dept of Internal Medicine


    Medical Faculty of Udayana University, Sanglah Central Public Hospital
    Denpasar 2018
    Disorders of the Immune System

     Hypersensitivity reactions
     Autoimmune diseases
     Immunologic deficiency syndromes
    HYPERSENSITIVITY
    Hypersensitivity reactions
    A reflection of excessive or abberant immune
    responses.
    The Classifications
    (Gell & Coombs)

     Type I (Immediate hypersensitivity)


     Type II (Cytotoxic / Ab-mediated hypersensitivity)
     Type III (Immune complex mediated hypersensitivity)
     Type IV (Delayed Type Hypersensitivity, Cell Mediated Immunity)
    1. Tipe I (Immediate hypersensitivity)

    (Abbas AK, 2010)


    PATHOPHYSIOLOGY
    •Anaphylactic reaction (IgE mediated reaction)

    Anaphylactic reaction / IgE mediated reaction3


    • Anaphylactoid reaction (Non IgE mediated)
    - Complement activation - Physical factors
    - Substance for Histamine released - Idiopathic
    - Arachidonic acid modulation
    (Roitt I, 1996)
    The action of Mast Cells Mediator in Immediate / Type I
    Hypersensitivity
    Action Mediator
    Vasodilation, increased vascular Histamine
    permeability PAF
    Leukotrienes C4, D4, E4
    Neutral proteases that activate
    complement and kinins
    Protaglandin D2
    Smooth muscle spasm Leukotrienes C4, D4, E4
    Histamine
    Prostaglandins
    PAF
    Cellular infiltration Cytokines, e.g., TNF
    Leukotriene B4
    Eosinophil and neutrophil chemotactic
    factors (not defined biochemically)
    PAF

    (Robbins & Cotran 2010)


    2. Cytotoxic / Antibody mediated
    (Type II Hypersensitivity)

    (Abbas AK, 2010)


    3. Immune Complex-Mediated (Type III) Hypersensitivity

    (Massoud Mahmoudi, 2008)


    4. Cell-Mediated (Type IV) Hypersensitivity

    Mechanism of T cell-mediated (type IV) hypersensitivity reactions.


    A. In delayed type hypersensitivity reactions, CD4+ T cells (and sometimes CD8+ cells)
    respond to tissue antigens by secreting cytokines that stimulate inflammation and
    activates phagocytes, leading to tissue injury.
    B. In some disease, CD8+ cytolytic T lymphocytes (CTLs) directly kill tissue cells.
    APC, antigen-presenting cell.
    (Abbas AK,
    Type of hypersensitivity diseases
    Type of hypersensitivity Pathologic immune Mechanisms of tissue
    mechanisms Injury & disease
    Immediate IgE antibody Mast cells & their mediators
    Hypersensitivity : (vasoactive amines, lipid mediators,
    Type I cytokines).

    Antibody mediated: Type II IgM, IgG antibodies against Opsonization & phagocytosis of
    cell surface or extracellular cells. Complement- & Fc receptor
    matrix antigens mediated recruitment & activation
    of leukocytes (neutrophils,
    macrophages). Abnormalities in
    cellular functions
    (eg; hormone receptor signaling).

    Immune complex Immune complexes of Complement- & Fc receptor


    Mediated : Type III circulating antigens & IgM mediated recruitment & activation
    or IgG antibodies. of leukocytes.
    T cell mediated : Type IV 1. CD4+ T cells (delayed 1. Macrophage activation,
    type hypersensitivity) cytokine-mediated
    2. CD8+ CTLs (T cell- inflammation.
    mediated cytolysis) 2. Direct target cell killing,
    cytokine-mediated
    inflammation

    (Abbas AK, 2010)


    Mechanisms of Immunologically Mediated diseases
    Type Prototype Disorder Immune Mechanism Pathologic Lesions

    Immediate (type I) Anaphylaxis; bronchial Production of IgE antibody  Vascular dilation, edema,
    hypersensitivity asthma (atopic forms) immediate release of vasoactive smooth muscle
    amines and other mediators from contraction,
    mast cells; recruitment of
    mucus production.
    inflammatory cells (late-phase
    reaction) Inflammation

    Antibody-mediated Autoimmune hemolytic Production of IgG, IgM  binds to Cell lysis, inflammation
    (type II) hypersensitivity anemia; Goodpasture antigen on target cell or tissue 
    phagocytosis or lysis of target cell
    syndrome
    by activated complement of Fc
    receptors; recruitment of
    leukocytes

    Immune complex Systemic lupus Deposition of antigen  antibody Necrotising vasculitis


    mediated (type III) erythematosus; complexes  complement (fibrinoid necrosis);
    hypersensitivity Some forms of activation  recruitment of inflammation
    leukocytes by complement
    glomerulonephritis;
    products and Fc receptors 
    serum sickness; release of enzyme and other toxic
    Arthus reaction molecules

    Cell-mediated (type IV) Contact dermatitis; Activated T lymphocytes  Perivascular cellular


    hypersensitivity multiple sclerosis; i) release of cytokines and infiltrates,
    type I diabetes; macrophage activation; edema;
    transplant rejection; ii) T cell-mediated cytotoxicity cell destruction;
    tuberculosis granuloma formation

    (Robbins and Cotran, 2010)


    Clinical Syndrome and Therapy
    Clinical Clinical & pathologic Therapy Mechanism of action
    syndrome manifestations
    Anaphylaxis Shock caused by vascular Epinephrine Vascular smooth muscle contraction;
    dilatation, Increases cardiac output ( to counter
    Airway obstraction due to laryngeal shock ); inhibits further mast cell
    adema degranulation

    Bronchial Bronchial hyper- Bronchodilators Relax bronchial smooth muscles


    asthma responsiveness caused by Corticosteroids Reduce inflammation
    smooth muscle contraction;
    Inflammation & tissue injury
    caused by late phase reaction
    Most allergic Due to the clinical syndrome Desensitization Unknown; may inhibit IgE production
    diseases (repeated & increase production other Ig, induce
    administration of low T cell tolerance
    doses of allergens)

    Anti-IgE Antbody Neutralize & eliminate IgE


    Antihistamines Block action of histamine on vessels
    & smooth muscles
    Cromolyn Inhibits mast cell degranulation
    (Abbas AK, 2010)
    Summary

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