Abstract
Activation of neutrophils by the interaction of immune complexes with Fc gamma receptors (FcγR) is amplified in tumor necrosis factor-alpha (TNFα)-primed cells, whereas interleukin-10 (IL-10) has been reported to suppress cytokine-mediated neutrophil activation. We examined whether the expression and function of FcγR in human neutrophils is modulated by TNFα and IL-10 in vitro, and whether FcγRIIa expression is altered following treatment with the TNFα inhibitor infliximab in rheumatoid arthritis (RA) patients in vivo. TNFα treatment induced upregulation of expression and function of the major activating Fc receptor, FcγRIIa, in neutrophils from healthy donors. Unexpectedly, treatment with IL-10 led to gain of FcγRIIa function in TNFα-primed neutrophils. In neutrophils from RA patients initiating infliximab therapy and followed longitudinally through consecutive treatments, FcγRIIa protein decreased during the course of TNFα blockade, indicating that FcγRIIa is a target of TNFα modulation in human neutrophils in vivo.
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