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Departments of
*
Cell Processing and
Clinical Immunology and AIDS Research Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan; and
Japanese Red Cross Central Blood Center, Tokyo, Japan
We examined the effect of TGF-ß1 on the chemotactic migratory
ability of human monocyte-derived dendritic cells (DCs). Treatment of
immature DCs with TGF-ß1 resulted in increased expressions of CCR-1,
CCR-3, CCR-5, CCR-6, and CXC chemokine receptor-4 (CXCR-4), which were
concomitant with enhanced chemotactic migratory responses to their
ligands, RANTES (for CCR-1, CCR-3, and CCR-5), macrophage-inflammatory
protein-3
(MIP-3) (for CCR-6), or stromal cell-derived growth
factor-1 (for CXCR-4). Ligation by TNF- resulted in
down-modulation of cell surface expressions of CCR-1, CCR-3, CCR-5,
CCR-6, and CXCR-4, and the chemotaxis for RANTES, MIP-3, and stromal
cell-derived growth factor-1, whereas this stimulation up-regulated
the expression of CCR-7 and the chemotactic ability for MIP-3ß.
Stimulation of mature DCs with TGF-ß1 also enhanced TNF--induced
down-regulation of the expressions of CCR-1, CCR-3, CCR-5, CCR-6, and
CXCR-4, and chemotaxis to their respective ligands, while this
stimulation suppressed TNF--induced expression of CCR-7 and
chemotactic migratory ability to MIP-3ß. Our findings suggest that
TGF-ß1 reversibly regulates chemotaxis of DCs via regulation of
chemokine receptor expression.
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