TGF-beta regulation of human macrophage scavenger receptor CD163 is Smad3-dependent.
J Leukoc Biol
; 76(2): 500-8, 2004 Aug.
Article
em En
| MEDLINE
| ID: mdl-15136587
ABSTRACT
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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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Antígenos de Diferenciação Mielomonocítica
/
Antígenos CD
/
Transativadores
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Fator de Crescimento Transformador beta
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Receptores de Superfície Celular
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Proteínas de Ligação a DNA
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Macrófagos
Limite:
Humans
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article