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11 Cards in this Set
- Front
- Back
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Components of an allergic response
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IgE
standard Ig structure .... |
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Mast cells and Basophils
both express high affiinity FcER both contain histamine, TNF-a, and leukotrienes in cytoplasm Mast cell- tissue bound, compartmentalized as mucosal or conn tissue, contain potent vasoactive compounds |
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Mast cells contain large amt of histamine, proteases, leukotriene B4 (LTG4), heparin and inflammatory cell cytokines that include IL 3, 4, 5, 6, 8, TNF-a, chemokines and GM-CSF.
When these cells release these very potent mediators, important conseq ensue |
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There is a direct relationship btwn serum IgE levls, allergic rxn and the atopic state.
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Genetic background
any allergen- almost anything can be an allergen but there is a trend towards proteins with enzymatic activity or ones that induce it. Timing is important: decreased early exposure to infections in genetically predisposed indivudiual is associated with insuffiicient T regulator control of IgE route- mucosal exposure predominated |
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Describe the sequence of the allergic response
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First exposure to antigen- usually mucosal (resp or GI) but can be cutaneous or systemic
extraction of antigen-by antigen presenting cells (DC) via "allergic" TLR that induces the DC to produce IL-4 instead of IL-12 presentation of the allergen as immunodominant peptide in a Class II MHC groove. Allergic reponses depend on Th2 activiation. Th2 cells prived the critical IL-4 signal to an allergen specific B cell accelerated prod of TH2 ctyokines espec IL3 and IL13 dominate Promotion of IgE calls switinch occurs upreglation of CD-23 on mast cells adn basophils that increase IL4 and IL 13 iL 4 from TH2, Basophils and mast cells active E germ line trx in B cells and results in IgE synthesis |
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What is the Late Phase Response
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Late phase response is secondary to the release of mediators of cells that were recruited to the site of massive degranulation.
Is completely dependent on T-cell activiation and presence of cytokines IL3, 4, 5,13, TNF-a, GM-CSF, and IL10 IL3, 5, GM-CSF amplify eosinophil production by bone marrow EOTAXIN Characterized by eosinophils |
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What are the clinical manifestations of an allergic response
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strongly dependent on the site of the reaction
anaphylaxis with laryngeal and brochiolar constriction and generalized increase in vascular. They can be fatal. Allergic rhinitis Hives (urticaria) - skin lesions occur when IgE armed mast cells are activated in skin Acute and chronic bronchial asthma occurs when IgE armed cells are recruited to submucosal sites of the pulmonary bronchi |
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Asthma
see fig 10.18 |
genetic predisposition
environmental condition (right allergen at right time, small fam = hygiene hypothesis, etc.) T reg cell deficiency Atopy Triggers lead to IgE antibodies leads to allergic syndromes |
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Why is there are marked increase in asthma in the industrial world
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Hygiene Hypothesis
decr. childhood infection and later exposure early exposure to less see page 10 |
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RAST ASSAY
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Allergen in solid phase
IgE ()serum IgE binds to allergen radiolabeled anti-IgE only used in children of people who can't do the skin test |
