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22 Cards in this Set
- Front
- Back
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What is the immune mechanism for Type I Hypersensitivity?
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Allergen cross-links IgE antibody; release of vasoactive amines and other mediators from basophils and mast cells; recruitment of other inflammatory cells
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What are some examples of Type I Hypersensitivity?
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Anaphylaxis, some forms of bronchial asthma.
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What is the immune mechanism for Type II Hypersensitivity?
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IgG or IgM binds to antigen on cell surface; phagocytosis of target cell or lysis of target cell by complement of antibody-dependent cell-mediated cytotoxicity
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What are some examples of Type II Hypersensitivity?
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Autoimmune hemolytic anemia, erythroblastosis fetalis, Goodpasture disease, pemphigus vulgaris
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What is the immune mechanism for Type III Hypersensitivity?
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Antigen-antibody complexes; activate complement; attract neutrophils; release of lysosomal enzymes, oxygen free radicals, etc.
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What are some examples of Type III Hypersensitivity?
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Arthus reaction, serum sickness, systemic lupus erythematosus, certain forms of acute glomerulonephritis
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What is the immune mechanism for Type IV Hypersensitivity?
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Sensitized T lymphocytes; release of cytokines and T cell-mediated cytotoxicity
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What are some examples of Type IV Hypersensitivity?
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Tuberculosis, contact dermatitis, transplant rejection
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What are the two phases of localized type I reaction?
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1) The initial response, characterized by vasodilation, vascular leakage, and smooth muscle spasm (evident within 5 to 30 minutes, lasting for 60 minutes)
2) Second, late-phase reaction characterized by more intense infiltration of tissues with eosinophils and other acute and chronic inflammatory cells, as well as tissue destruction (sets in 2 to 8 hours later, lasts for several days) |
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What are primary mediators?
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Preformed mediators within mast cell granules that are released to initiate the early events in type I reactions. Histamine is the most important of these mediators, and causes increased vascular permeability, vasodilation, bronchoconstriction, increased secretion of mucus. Other mediators include adenosine, chemotactic factors for neutrophils and eosinophils, heparin and neutral proteases.
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What are secondary mediators?
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Arachidonic acid metabolites (lipid mediators) and cytokines that are synthesized de novo.
The lipid mediators are generated by activation of phospholipase A2, which leukotrienes and prostaglandins are synthesized from. Leukotrienes C4 and D4 are the most potent vasoactive and spasmogenic agents known. Platelet-activating factor results in platelet aggregation, histamine release, and bronchospasm, and is chemotactic for neutrophils and eosinophils. Mast cell-produced cytokines (TNF, IL-1, 4, 5, 6) and chemokines recruit and activate inflammatory cells. |
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Which mast cell mediators cause cellular infiltration?
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Cytokines
Leukotriene B4 Eosinophile and Neutrophil chemotactic factors Platelet-activating factor |
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Which mast cell mediators have vasoactive actions (vasodilation, increased vascular permeability)
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Histamine
Platelet-activating factor Leukotrienes C4, D4, E4 Neutral proteases that activate complement and kinins Prostaglandin D2 |
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Which mast cell mediators cause smooth muscle spasm?
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Leukotrienes C4, D4, E4
Histamine Prostaglandins Platelet-activating factor |
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What are the three different antibody-dependent mechanisms involved in type II reactions?
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Complement-dependent
Antibody-dependent cell mediated cytotoxicity Antibody-mediated cellular dysfunction |
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What occurs in complement-dependent reactions?
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There are two mechanisms: direct lysis and opsonization.
Clinically, antibody-mediated reactions occur in: Transfusion reactions (ABO antigens) Erythroblastosis fetalis (Rh factor) Autoimmune hemolytic anemia, agranulocytosis, or thrombocytopenia (antibodies against own blood cells) Drug reactions Pemphigus vulgaris (antibodies against desmosomal proteins lead to disruption of epidermal intercellular junctions) |
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What occurs in antibody-dependent cell-mediated cytotoxicity (ADCC)?
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Involves killing via cell types that bear receptors for the Fc portion of IgG; targets coated by antibody are lysed without phagocytosis or complement fixation.
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What occurs in antibody-mediated cellular dysfunction?
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Antibodies directed against cell surface receptors impair or dysregulate function without causing cell injury or inflammation.
Myasthenia gravis (inhibit ACh receptors) Graves disease (activate TSH receptor) |
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What is the pathogenesis of systemic immune complex disease (type III)
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1) Formation of antigen-antibody complexes in the circulation
2) Deposition of the immune complexes in various tissues 3) Inflammatory reaction in various sites |
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What two factors are important in determining whether the immune complex formation leads to disease?
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Size of the immune complex: very large complexes are rapidly removed from the circulation by MNPs, and are relatively harmless. The most pathogenic complexes are formed during antigen excess and are small or intermediate size.
Status of MNP system: overload or dysfunction of macrophages leads to persistence of immune complexes. |
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What is Arthus reaction?
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Localized area of tissue necrosis resulting from acute immune complex vasculitis (inflammatory destruction of blood vessels).
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What are the two types of type IV reactions?
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1) Delayed-type hypersensitivity, initiated by CD4+ T cells
2) Direct cell cytotoxicity, mediated by CD8+ T cells |
