Abstract
The mechanisms of tissue injury in immune complexes (IC) glomerulonephritis are incompletely understood. Most of studies have been dedicated to IgG IC. However, few data exist about the pathogenetic mechanisms of IgA mediated diseases. In this paper we have explored the possibility that neutrophils and mesangial cells exposed to IgA Immune complexes, can mediate the production of platelet activating factor (PAF) and oxygen radicals (OR).
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