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    Lecture 6 (2014) FMS 4

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    gio
    The document discusses the four types of hypersensitivity reactions. Type I reactions are immediate and IgE-mediated, involving mast cell and basophil degranulation upon allergen exposure. Type I reactions commonly cause allergic rhinitis and asthma.

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    Lecture 6 (2014) FMS 4

    Uploaded by

    gio
    20 views27 pages
    The document discusses the four types of hypersensitivity reactions. Type I reactions are immediate and IgE-mediated, involving mast cell and basophil degranulation upon allergen exposure. Type I reactions commonly cause allergic rhinitis and asthma.

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    lecture 6 (2014) FMS 4

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    The document discusses the four types of hypersensitivity reactions. Type I reactions are immediate and IgE-mediated, involving mast cell and basophil degranulation upon allergen exposure. Type I reactions commonly cause allergic rhinitis and asthma.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    20 views27 pages

    Lecture 6 (2014) FMS 4

    Uploaded by

    gio
    The document discusses the four types of hypersensitivity reactions. Type I reactions are immediate and IgE-mediated, involving mast cell and basophil degranulation upon allergen exposure. Type I reactions commonly cause allergic rhinitis and asthma.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    You are on page 1of 27

    Introduction

     Excessive or inappropriate immune response


    sometimes lead to host tissue damage

     Resulting from prolonged or repeated


    antigen exposure

     These reactions called hypersensitivity


    reactions
    Hypersensitivity reactions

     These reactions are classified into 4


     Type I
     Type II Antibody Dependent
     Type III
     Type IV Antibody Independent
    Type I hypersensitivity

     Commonly called allergic or immediate


    hypersensitivity reactions

     Occurs within minutes to hours of antigen


    exposure

     Some individuals develop IgE antibodies in


    response to relatively harmless
    environmental antigens or allergens
    Type I hypersensitivity

     Allergen
     Nonparasitic antigen
    capable of stimulating
    type I hypersensitivity
    in allergic individuals
    Type I hypersensitivity
     IgE molecules bind to Fc receptors (FcRε) on
    the surfaces of mast cells and basophils
     IgE-FcRε complexes
    Allergen
     Degranulations
     Release of vasoactive amine (histamine) and
    other inflammatory mediators
    Type I
    hypersensitivit
    y
    Type I hypersensitivity
    Type I hypersensitivity
    Type I hypersensitivity
    Type I hypersensitivity
    Type I hypersensitivity

     Localized reactions
     Mast cells accumulate in respiratory passages ,
    intestinal walls, and the skin
     Type 1 reactions are often most pronounced in
    these tissues
     Example:
     Antigen enter the body by inhalation
     Localize primarily to the nasopharyngeal and
    bronchial tissue
     Smooth muscle contraction and vasodilation
     Asthma
    Type I hypersensitivity
     Systemic reactions
     Anaphylaxis reaction
    Type II hypersensitivity

     Initiated by the interaction of antibody (IgM


    or IgG) with cell membranes or with the
    extracellular matrix
    Type II hypersensitivity
     ADCC (Antibody dependent cell mediated
    cytotoxicity)
    Type II hypersensitivity

     Complement activation (classical pathway)


    Type II hypersensitivity
     Complement activation (classical pathway)
    Type II hypersensitivity

     Antibody-mediated disruption of cellular


    function
    Type II hypersensitivity

     Example of type II hypersensitivity reaction


    Type III hypersensitivity

     Circulating antigen-antibody complexes may


    lead to inflammation at their sites of
    deposition

     Often the complexes are deposited mainly in


    small arteries, renal glomeruli, and the
    synovia joints
    Type III hypersensitivity

    TYPE II

    TYPE III
    Type III hypersensitivity
     Localized reactions
     Arthus reactions
     Systemic reactions
     Serum sickness
    Type IV hypersensitivity

     Result from the interaction of T cell-initiated


    inflammation and do not involve antibody

     The manifestation is late (48-72 after


    exposure)
    Question
    A 12-year-old girl develops symptoms of sneezing, runny nose, and
    itchy eyes when she is near cat. This patient has symptoms consistent
    with allergic rhinitis due to cat dander. What is the underlying
    mechanism for this clinical finding?
    a. Crosslinking of receptor-bound IgE antibody by the allergen (cat
    dander) activates neutrophils
    b. Crosslinking of receptor-bound IgE antibody by the allergen (cat
    dander) activates mast cells
    c. Crosslinking of receptor-bound IgG antibody by the allergen (cat
    dander) activates neutrophils
    d. Crosslinking of receptor-bound IgG antibody by the allergen (cat
    dander) activates mast cells
    e. Crosslinking of receptor-bound IgA antibody by the allergen (cat
    dander) activates mast cells

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