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J. Exp. Med.,
Volume 188, Number 1, July 1, 1998 217-222
Receptor Type I
By
From the * Department of Microbiology and Immunology, Temple University School of Medicine,
Philadelphia, Pennsylvania 19140; and the Macrophages can respond to a variety of infectious and/or inflammatory stimuli by secreting an
array of proinflammatory cytokines, the overproduction of which can result in shock or even
death. In this report, we demonstrate that ligation of macrophage Fc Department of Pediatrics, Cornell University Medical
College, New York 10021
receptors (FcR) can
lead to a reversal of macrophage proinflammatory responses by inducing an upregulation of interleukin (IL)-10, with a reciprocal inhibition of IL-12 production. IL-10 upregulation was
specific to FcR ligation, since the ligation of the Mac-1 receptor did not alter IL-10 production. The identification of the specific FcR subtype responsible for IL-10 upregulation was determined in gene knockout mice. Macrophages from mice lacking the FcR chain, which is
required for assembly and signaling by FcRI and FcRIII, failed to upregulate IL-10 in response to immune complexes. However, mice lacking either the FcRII or the FcRIII were
fully capable of upregulating IL-10 production, implicating FcRI in this process. The biological consequences of FcRI ligation were determined in both in vitro and in vivo models of inflammation and sepsis. In all of the models tested, the ligation of FcR promoted the production of IL-10 and inhibited the secretion of IL-12. This reciprocal alteration in the pattern of
macrophage cytokine production illustrates a potentially important role for FcR-mediated
clearance in suppressing macrophage proinflammatory responses.
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