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Originally published online as doi:10.1189/jlb.1203617 on May 10, 2004

Published online before print May 10, 2004
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(Journal of Leukocyte Biology. 2004;76:500-508.)
© 2004 by Society for Leukocyte Biology

TGF-ß regulation of human macrophage scavenger receptor CD163 is Smad3-dependent

Patricia A. Pioli1, Katie E. Goonan, Kathleen Wardwell and Paul M. Guyre

Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire

1Correspondence: Department of Physiology, Dartmouth Medical School, Lebanon, NH 03756. E-mail: pioli{at}dartmouth.edu

Tight regulation of the inflammatory response is essential for the maintenance of physiologic homeostasis. A potentially important mediator of this process is CD163, a macrophage-specific member of the scavenger receptor cysteine-rich family. CD163 surface expression is up-regulated by glucocorticoids and the anti-inflammatory cytokine interleukin-10, and CD163 is shed acutely from the cell surface in response to lipopolysaccharide. We now demonstrate that transforming growth factor-ß (TGF-ß) markedly reduces expression of CD163. Treatment of primary human monocytes with TGF-ß inhibited basal as well as dexamethasone-induced CD163 mRNA and protein expression. De novo protein synthesis was not required for this inhibition, suggesting that TGF-ß regulates CD163 expression transcriptionally. To delineate this transcriptional regulation, a 2.5-kb fragment of the CD163 promoter was isolated. This promoter was inhibited by TGF-ß, and suppression was dependent on Smad3 expression. These results define a novel function for TGF-ß and implicate an important role for CD163 in the host response to inflammation.

Key Words: cytokine • inflammation • glucocorticoid • signal transduction




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