BIO 447 Lecture Notes - Lecture 10: Interleukin 4, Phospholipid, Interleukin 3

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21 Dec 2017
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Allergen/immunogen, dose of allergen, route of exposure/administration, host genetics. Atopic allergy: genetic mis-regulation of ige production or response. Immediate hypersensitivity: within minutes (type i) or hours (type ii and iii) Ag induces cross-linking of ige bound to mast cells/basophils causes release of vasoactive mediators. Non ige initiators of type i hypersensitivity: complement activation products, anaphylotoxins: c3a, c4a, c5a, drugs: acth, codeine, morphine, penicillin. The process: initially - caused by prior sensitization that results in immune response, mediated by cd4+ lymphocytes promote mast cell/plasma cell production of ige. To treat type i immediate hypersensitivity: block effects of primary mediators on target cells (respiratory smooth muscles, vascular endothelium, block the binding of his to receptors - Antihistamines, cortisone: block ca2+ ion influx (cromolyn, block effects of ca2+ ion influx, keep camp from falling (theophylline) Increased camp production (adrenaline: hyposensitization repeated injections of increasing doses of allergen, shift from ige to igg production or induce t-cell mediated suppression.

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