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Ocul Immunol Inflamm：Vogt-Koyanagi-Harada（VKH）疾病中TGR5的表达下降

2019-02-28 不详 网络

Vogt-Koyanagi-Harada疾病机制TGR5
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重庆市第一附属医院重庆眼科研究所的Yang J等人近日在Ocul Immunol Inflamm杂志上发表了一篇重要的研究论文，他们研究了G蛋白偶联胆汁酸受体-1，Gpbar1（TGR5）在Vogt-Koyanagi-Harada（VKH）疾病发病机制中的作用。

重庆市第一附属医院重庆眼科研究所的Yang J等人近日在Ocul Immunol Inflamm杂志上发表了一篇重要的研究论文，他们研究了G蛋白偶联胆汁酸受体-1，Gpbar1（TGR5）在Vogt-Koyanagi-Harada（VKH）疾病发病机制中的作用。

他们通过实时PCR测定巨噬细胞中TGR5、iNOS、Arg1、CD16和CD206的mRNA水平。使用ELISA来检测细胞培养上清液中细胞因子。通过流式细胞术测试CD4 + IFN-γ+和CD4 + IL-17 + T细胞的阳性率。

研究发现，与正常对照相比，在活性VKH患者中观察到M1巨噬细胞中TGR5的表达降低。用INT-777刺激M1巨噬细胞的TGR5引起炎性M1向抗炎M2巨噬细胞亚型的转变。与CD4 + T细胞共培养的巨噬细胞的TGR5活化抑制Th1和Th17极化。同时发现，培养上清液中IFN-γ和IL-17被释放。

因此，他们认为，其结果表明TGR5表达降低可能有助于VKH疾病的发病进展。

原文出处：

Yang， J.， et al.， Decreased Expression of TGR5 in Vogt-Koyanagi-Harada (VKH) Disease. Ocul Immunol Inflamm， 2019： p. 1-9

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