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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 (Fc
R) 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 Fc
R ligation, since the ligation of the Mac-1 receptor did not alter IL-10 production. The identification of the specific Fc
R 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 Fc
RI and Fc
RIII, failed to upregulate IL-10 in response to immune complexes. However, mice lacking either the Fc
RII or the Fc
RIII were
fully capable of upregulating IL-10 production, implicating Fc
RI in this process. The biological consequences of Fc
RI ligation were determined in both in vitro and in vivo models of inflammation and sepsis. In all of the models tested, the ligation of Fc
R 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 Fc
R-mediated
clearance in suppressing macrophage proinflammatory responses.
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