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首页> 外文期刊>Cellular Signalling >TNF family molecule LIGHT regulates chemokine CCL27 expression on mouse embryonic stem cell-derived dendritic cells through NF-kappa B activation
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TNF family molecule LIGHT regulates chemokine CCL27 expression on mouse embryonic stem cell-derived dendritic cells through NF-kappa B activation

机译：TNF家族分子LIGHT通过NF-κB激活调节小鼠胚胎干细胞来源的树突状细胞上趋化因子CCL27的表达

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Cytokine LIGHT is a type II transmembrane protein belonging to the TNF family that was originally identified as a weak inducer of apoptosis. It plays a role in inducing maturation of dendritic cells, such as upregulating CD80, CD86 expression on dendritic cells. However, whether LIGHT induces CC chemokine expression in DC and promotes their migration remains unknown. In this study, we found that esDC express CCR7 and CCR10 (the receptor of CCL27) upon the LIGHT stimulation. LIGHT also upregulates CCL27, but not CCL19 and CCL21 expression in esDC. The esDC migration potential has been increased in LIGHT activated DCs compared with control cells. LIGHT activated DCs autocrine CCL27 which regulate their migration as Blockage of CCL27 on esDC using neutralizing antibody reduces migration potential. In signaling study, we identified that LIGHT activated NF-kappa B in esDC and inhibition of NF-kappa B activation by specific inhibitor can partly attenuate the effect of LIGHT in regulation of CCL27 expression. Moreover, Shp-2 is required in LIGHT activated NF-kappa B because Knockdown of Shp-2 affects the NF-kappa B activation induced by LIGHT and consequently influences LIGHT mediated CCL27 expression. TRAF6 is critical in DC maturation in recent reports; however, knockdown of TRAF6 expression using siRNA did not alter CCL27 expression in LIGHT matured DCs. Our study demonstrates that LIGHT stimulation enhances CCL27 expression through activation of NF-kappa B in DCs. (c) 2006 Elsevier Inc. All rights reserved.
机译：细胞因子LIGHT是属于TNF家族的II型跨膜蛋白，最初被鉴定为细胞凋亡的弱诱导剂。它在诱导树突状细胞的成熟中起作用，例如上调CD80，CD86在树突状细胞上的表达。然而，LIGHT是否在DC中诱导CC趋化因子表达并促进其迁移尚不清楚。在这项研究中，我们发现esDC在LIGHT刺激下表达CCR7和CCR10（CCL27的受体）。 LIGHT还上调esDC中的CCL27，但不上调CCL19和CCL21的表达。与对照电池相比，在LIGHT激活的DC中esDC的迁移潜力有所增加。 LIGHT激活的DC自分泌CCL27，可调节其迁移，因为使用中和抗体对esDC上CCL27的阻断可降低迁移潜力。在信号研究中，我们确定了LIGHT在esDC中激活了NF-κB并通过特异性抑制剂抑制NF-κB的激活可以部分减弱LIGHT在调节CCL27表达中的作用。而且，Shp-2在LIGHT激活的NF-κB中是必需的，因为Shp-2的敲低会影响LIGHT诱导的NF-κB激活，从而影响LIGHT介导的CCL27表达。在最近的报道中，TRAF6对于DC成熟至关重要。然而，使用siRNA抑制TRAF6表达不会改变LIGHT成熟DC中CCL27的表达。我们的研究表明，光刺激通过激活DC中的NF-κB增强CCL27的表达。 （c）2006 Elsevier Inc.保留所有权利。

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