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The Journal of Immunology, 1999, 162: 7041-7048.
Copyright © 1999 by The American Association of Immunologists

Reactive Oxygen Intermediates Enhance Fc{gamma} Receptor Signaling and Amplify Phagocytic Capacity1

Luminita Pricop, Jayashree Gokhale, Patricia Redecha, Sonia C. Ng and Jane E. Salmon2

Department of Medicine, Hospital for Special Surgery and New York Presbyterian Hospital, Graduate Program in Immunology, Weill Medical College of Cornell University, New York, NY 10021

Receptors for the Fc region of IgG (Fc{gamma}R) mediate internalization of opsonized particles by human neutrophils (PMN) and mononuclear phagocytes. Cross-linking of Fc{gamma}R leads to activation of protein tyrosine kinases and phosphorylation of immunoreceptor tyrosine-based activation motifs (ITAMs) within Fc{gamma}R subunits, both obligatory early signals for phagocytosis. Human PMN constitutively express two structurally distinct Fc{gamma}R, Fc{gamma}RIIa and Fc{gamma}RIIIb, and can be induced to express Fc{gamma}RI by IFN-{gamma}. We have previously shown that stimulation of PMN through Fc{gamma}RIIIb results in enhanced Fc{gamma}RIIa-mediated phagocytic activity that is inhibited by catalase. In the present study, we have tested the hypothesis that reactive oxygen intermediates (ROI) have the capacity to regulate Fc{gamma}R responses and defined a mechanism for this effect. We show that H2O2 augmented phagocytosis mediated by Fc{gamma}RIIa and Fc{gamma}RI in PMN and amplified receptor-triggered tyrosine phosphorylation of Fc{gamma}R-associated ITAMs and signaling elements. Generation of endogenous oxidants in PMN by cross-linking Fc{gamma}RIIIb similarly enhanced phosphorylation of Fc{gamma}RIIa and Syk, a tyrosine kinase required for phagocytic function, in a catalase-sensitive manner. Our results provide a mechanism for priming phagocytes for enhanced responses to receptor-driven effects. ROI generated in an inflammatory milieu may stimulate quiescent cells to rapidly increase the magnitude of their effector function. Indeed, human monocytes incubated in the presence of stimulated PMN showed oxidant-induced increases in Fc{gamma}RIIa-mediated phagocytosis. Definition of the role of oxidants as amplifiers of Fc{gamma}R signaling identifies a target for therapeutic intervention in immune complex-mediated tissue injury.




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