Abstract
Recent advances in our understanding of the mechanisms that regulate acute and chronic inflammatory responses have revealed a key role for reactive oxygen intermediates in modulating the activation of neutrophils. Opsonized microbes and immune complexes initiate the oxidative burst by the engagement of receptors for immunoglobulin G, termed Fcγ receptors. The regulation of phagocytic cell function by oxidant-sensitive signaling pathways optimizes host defense capabilities, but it also amplifies tissue damage. This review will focus on the cross-talk between Fcγ receptors and reactive oxygen intermediates at sites of inflammation and its role in microbial immunity.
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