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6 Cards in this Set

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The antigen penetrates the host's primary defenses eg skin, mucous, thus exposing itself to the mediators of the host's secondary defenses. This constitutes the first exposure.
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The antigen is recognized by one of the membrane-bound immunoglobulins on the B cell surface. The B cell internalizes, processes and expresses a portion of the antigen via MHC2 receptors. Presentation of the antigen by MHC2 to the TCR of the T cell results in activation of Th-2 cells, which produces several cytokines, including IL-2, (T and B cell proliferation) and IL-2 (B cell affinity maturation and production of IgE)
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The B cell then becomes immunoglobulins secreting machines known as plasma cells, pumping out vast quantities of single immunoglobulins isotype. In the case of hypersensitivity, the IgE isotype is of particular interest.
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Mast cells contain many vesicles filled with the mediators of hypersensitivity reactions intracellularly. Extracellulary these cells express FcR1 receptors, which bind to the Fc portions of IgE prior to second antigen exposure. At this point, the mast cell may be considered charged with the potential to instigate a hypersensitivty reaction.
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Upon second exposure to the antigen, the IgE molecules bound to the charged mast cell, recognize and bind the same portions of the antigen.
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Antigen bound IgE molecules cause cross-linking of mast cell FcR1 molecules, resulting in activation and subsequent degranulation of mast cells. The granules released into the interstitium constitute the fuel for hypersensitivity reactions and can be generalized into two types. Immediate phase hypersensitivity is mediated by proteins and amines (Eg histamine) and results in the classic wheal and flare reaction in minutes after exposure. Late phase hypersensitivity is mediated by cytokines, which induce a storm of inflammatory leukocytes (Eg neutrophils, eosinophils, basophils) 2-4 hours after the immediate phase. Inflammation typically peaks at 24 hours and subsides gradually thereafter.
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