Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 76, Issue 2, Pages 500-508Publisher
FEDERATION AMER SOC EXP BIOL
DOI: 10.1189/jlb.1203617
Keywords
cytokine; inflammation; glucocorticoid; signal transduction
Categories
Funding
- NCRR NIH HHS [RR16437] Funding Source: Medline
- NIAID NIH HHS [AI51877, AI051547, AI053243] Funding Source: Medline
- NIDDK NIH HHS [DK07508] Funding Source: Medline
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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-beta (TGF-beta) markedly reduces expression of CD163. Treatment of primary human monocytes with TGF-beta 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-beta 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-beta, and suppression was dependent on Smad3 expression. These results define a novel function for TGF-beta and implicate an important role for CD163 in the host response to inflammation.
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