J. Exp. Med.
© The Rockefeller University Press
0022-1007/97/06/1977/09 $2.00
Volume 185, Number 11, June 2, 1997 1977-1985

Selective Suppression of Interleukin-12 Induction after Macrophage Receptor Ligation

By Fayyaz S. Sutterwala,^* Gary J. Noel, Raphael Clynes,^§ and David M. Mosser^*

From the ^* Department of Microbiology and Immunology,  Temple University School of Medicine, Philadelphia, Pennsylvania 19140; the  Department of Pediatrics, Cornell University Medical College, New York,10021; and the ^§ Laboratory of Molecular Genetics and Immunology, Rockefeller University, New York, 10021

Interleukin (IL)-12 is a monocyte- and macrophage-derived cytokine that plays a crucial role in both the innate and the acquired immune response. In this study, we examined the effects that ligating specific macrophage receptors had on the induction of IL-12 by lipopolysaccharide (LPS). We report that ligation of the macrophage Fc, complement, or scavenger receptors inhibited the induction of IL-12 by LPS. Both mRNA synthesis and protein secretion were diminished to near-undetectable levels following receptor ligation. Suppression was specific to IL-12 since IL-10 and tumor necrosis factor- (TNF-) production were not inhibited by ligating macrophage receptors. The results of several different experimental approaches suggest that IL-12 downregulation was due to extracellular calcium influxes that resulted from receptor ligation. First, preventing extracellular calcium influxes, by performing the assays in EGTA, abrogated FcR-mediated IL-12(p40) mRNA suppression. Second, exposure of macrophages to the calcium ionophores, ionomycin or A23187, mimicked receptor ligation and inhibited IL-12(p40) mRNA induction by LPS. Finally, bone marrow-derived macrophages from FcR  chain-deficient mice, which fail to flux calcium after receptor ligation, failed to inhibit IL-12(p40) mRNA induction. These results indicate that the calcium influxes that occur as a result of receptor ligation are responsible for inhibiting the induction of IL-12 by LPS. Hence, the ligation of phagocytic receptors on macrophages can lead to a dramatic decrease in IL-12 induction. This downregulation may be a way of limiting proinflammatory responses of macrophages to extracellular pathogens, or suppressing the development of cell-mediated immunity to intracellular pathogens.

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