Redox regulation of Fcgamma receptor-mediated phagocytosis: implications for host defense and tissue injury.
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 Fcgamma 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 Fcgamma receptors and reactive oxygen intermediates at sites of inflammation and its role in microbial immunity.
Pricop
Luminita
L
Hospital for Special Surgery and Weill Medical College of Cornell University, Department of Medicine, New York, NY 10021, USA.
Salmon
Jane E
JE
D000483:Alleles; D006801:Humans; D008954:Models, Biological; D010084:Oxidation-Reduction; D010587:Phagocytosis; D010766:Phosphorylation; D017452:Receptors, IgG / Q000378:metabolism*; D016897:Respiratory Burst; D015398:Signal Transduction; D013997:Time Factors
D017452:Receptors, IgG