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Receptors1
Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140
Our laboratory has previously demonstrated that the
ligation of phagocytic receptors on macrophages can influence cytokine
production. In this study, we examine the cytokine responses to
multiple inflammatory stimuli following Fc
R ligation. Macrophages
were stimulated in vitro with LPS, lipoteichoic acid, CD40 ligand, or
low molecular mass hyaluronic acid. All of these stimuli were
proinflammatory in character, inducing the production of high levels of
IL-12, but only modest amounts of IL-10. The coligation of FcR along
with these stimuli resulted in an anti-inflammatory profile,
abrogating IL-12 production and inducing high levels of IL-10. The
modulation of these two cytokines occurred by two independent
mechanisms. Whereas the abrogation of IL-12 biosynthesis was a property
shared by several macrophage receptors, the induction of IL-10 was
specific to the FcR. The biological relevance of these observations
was examined in murine models of endotoxemia, in which FcR ligation
induced the rapid production of IL-10 and prevented IL-12 synthesis.
Mice could be passively immunized with Abs to LPS to reverse
inflammatory cytokine production, and the transfer of macrophages whose
FcR had been ligated could rescue mice from lethal endotoxemia.
Thus, the ligation of the macrophage FcR can be exploited to prevent
inappropriate inflammatory cytokine responses.
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