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1 Suppresses Myeloid Fc
Receptor Function by Regulating the Expression and Function of the Common -Subunit1
* Department of Internal Medicine and Dorothy M. Davis Heart and Lung Research Institute, and The James Cancer Hospital and Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210
We have previously reported that Fc
R-mediated function in myeloid cells is a tightly regulated event that is influenced by the cytokines present in the milieu. TGF-
1 is an immunosuppressive cytokine with pleiotropic effects on immune responses; however, the molecular mechanism by which TGF- suppresses immune responses is poorly understood. In this study, we have analyzed the effect of TGF- on FcR-mediated activation of myeloid cells. We report that TGF-1-treated THP-1 human myeloid cells displayed reduced ability to phagocytose IgG-coated particles. Because FcR expression is modulated by cytokines, we analyzed expression levels of FcRI, FcRIIa, FcRIIb, and FcRIIIa in cells cultured with or without TGF-1 and found while total protein levels of the FcR were not reduced, surface expression of FcRI and FcRIII was lower in cells cultured with TGF-1. Concomitantly, there was a dose-dependent reduction in the expression of the FcR-associated -subunit. This suppressive effect of TGF- was likewise observed in bone marrow-derived murine myeloid cells and human monocytes. Importantly, TGF-1 also significantly reduced the production of monocyte chemoattractant protein-1 induced by immobilized IgG, which would further reduce monocyte recruitment to the site of inflammation. In contrast, human alveolar macrophages were refractory to this effect, expressing low levels of TGF- type II receptors compared with peripheral blood monocytes from the same donor. These data provide insight into the regulation of immune responses by TGF-1 and demonstrate the selectivity of these effects.
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