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S8C9VA1-3: Additional features that might be indicative of a role for B-cells are listed. |
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B-lymphocyte 4. histologic correlates: a. promote lysis and coagulation, or even atrophy, of target cells (mostly in cell-poor patterns) b. activation of complement, and emergence of complement cascade (neutrophilia, leukocytoclasia, edema, thrombosis, etc.) c. immunostimulation (i.e., lymphoepithelial islands as seen in Sjogren’s syndrome; somewhat similar lesions may involve sweat glands) |
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S8C9VA1-4: B lymphocytes are important in the mediation of immune responses; they have a role in the vascular phenomena associated with inflammation. Not all lymphoepithelial islands are representative of an interaction between B cells and epithelial cells. In some examples, T cells interact with epithelial cells. |
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Vasculitides 1. leukocytoclastic (neutrophilic and lymphocytic) 2. thrombotic 4. fixed a. pleomorphic and vasoproliferative (granuloma faciale) b. necrotizing and leukocytoclastic (erythema elevatum diutinum) |
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S8C9VA1-5: Variants in the general category of the vasculitides are listed. |
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Immune Complex Disease serum sickness (classic): a. systemic (circulating soluble complexes) b. diffusion of complexes d. antigen excess (soluble complex) |
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S8C9VA1-6: Features of serum sickness are listed. Serum sickness is commonly cited as a model for vasculitic disorders. |
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Immune Complex Disease a. damage at sites of localization of complexes (vasculitis, glomerulonephritis, alveolitis, synovitis) b. chemotaxis c. necrosis (leukocytoclasia, fibrinoid, thrombosis, hemorrhages) |
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S8C9VA1-7: Vascular phenomena, as encountered in the setting of serum sickness, are listed.
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