TGF-β1 reciprocally controls chemotaxis of human peripheral blood monocyte-derived dendritic cells via chemokine receptors
TGF-β1 reciprocally controls chemotaxis of human peripheral blood monocyte-derived dendritic cells via chemokine receptors
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DOI：
10.4049/jimmunol.164.5.2285
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发表时间：
2000-03-01
影响因子：
4.4
通讯作者：
Takahashi, TA
中科院分区：
文献类型：
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作者：
Sato, K;Kawasaki, H;Takahashi, TA
我们检测了转化生长因子-β1对人单核细胞来源的树突状细胞(DC)趋化迁移能力的影响。未成熟DC经转化生长因子-β1处理后，CCR-1、CCR-3、CCR-5、CCR-6和CXC趋化因子受体-4(CXCR-4)的表达增加，同时对其配体RANTES(针对CCR-1、CCR-3和CCR-5)、巨噬细胞炎症蛋白-3α(MIP-3α)(针对CCR-6)或基质细胞衍生生长因子-1α(针对CXCR-4)的趋化迁移反应增强。经肿瘤坏死因子-α处理后，细胞表面CCR-1、CCR-3、CCR-5、CCR-6和CXCR-4的表达下调，RANTES、MIP-3α和基质细胞衍生生长因子-1α的趋化能力增强，而CCR-7的表达和对MIP-3β的趋化能力增强。TGP-β1刺激成熟DC也增强了肿瘤坏死因子-α诱导的CCR-1、CCR-3、CCR-5、CCR-6和CXCR-4的表达下调以及对其相应配体的趋化作用，而这种刺激抑制了肿瘤坏死因子-α诱导的CCR-7的表达和对MIP-3β的趋化迁移能力。我们的研究结果表明，转化生长因子-β1通过调节趋化因子受体的表达，可逆地调节DC的趋化作用。
We examined the effect of TGF-beta 1 on the chemotactic migratory ability of human monocyte-derived dendritic cells (DCs). Treatment of immature DCs with TGF-beta 1 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 alpha (MIP-3 alpha) (for CCR-6), or stromal cell-derived growth factor-1 alpha (for CXCR-4). Ligation by TNF-alpha 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 alpha, and stromal cell-derived growth factor-1 alpha, whereas this stimulation up-regulated the expression of CCR-7 and the chemotactic ability for MIP-3 beta. Stimulation of mature DCs with TGP-beta 1 also enhanced TNF-alpha-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-alpha-induced expression of CCR-7 and chemotactic migratory ability to MIP-3 beta. Our findings suggest that TGF-beta 1 reversibly regulates chemotaxis of DCs via regulation of chemokine receptor expression.