Pathology 3240A Lecture Notes - Lecture 8: Nephritis, Diabetes Mellitus Type 1, Immunoglobulin G

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Often represent excessive immune response to an ag. May result from autoimmunity, rxns to microbes, or rxn to environmental ags. Often chronic due to persistence of the ags and amplification of the immune response. Release of vasoactive amines (e. g. histamine) e. g. asthma, hayfever. Results from th2, which helps in activating ige-producing b cells/plasma cells. Ige molecs are attached to mast cells, which become aciv"d and degranulate (release histamine, leukotrienes, prostaglandins) when ige binds ag in a previously sensitized individual = allergic/atopic rxn. Lysis of cells e. g. transfusion rxns due to mismatched blood, thrombocytopenic purpura, goodpasture syndrome. Abs bind to self ags and then activ complement or bind to fc receptors on phagocytes. Thus circulating cells which are opsonized by the ab may be targeted by phagocytes. Other cells damaged secondary to complement activation and inflammation. Ag-ab complexes in circ are trapped in organs, producing injury by complement and neutrophil activation e. g. systemic lupus erythematosus, post-strep glomerulonephritis.

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