TGR5 在 Vogt-Koyanagi-Harada（VKH）病中的表达降低。
Decreased Expression of TGR5 in Vogt-Koyanagi-Harada (VKH) Disease.
机构信息
Chongqing Key Lab of Ophthalmology, Chongqing Eye Institute, The First Affiliated Hospital of Chongqing Medical University, Chongqing, P. R. China.
University Eye Clinic Maastricht, Maastricht, The Netherlands.
出版信息
Ocul Immunol Inflamm. 2020;28(2):200-208. doi: 10.1080/09273948.2018.1560477. Epub 2019 Feb 22.
: To investigate the role of G-protein-coupled bile acid receptor-1, Gpbar1 (TGR5) in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease.: The mRNA level of TGR5, iNOS, Arg1, CD16, and CD206 in macrophages was assayed by real-time PCR. ELISA was used to detect the production of cytokines in cell culture supernatants. The frequencies of CD4IFN-γ and CD4 IL-17 T cells were tested by flow cytometry.: A decreased expression of TGR5 in M1 macrophages was observed in active VKH patients as compared with normal controls. TGR5 stimulation of M1 macrophages with INT-777 caused a shift of the inflammatory M1 toward the anti-inflammatory M2 macrophage subtype. TGR5 activation of macrophages co-cultured with CD4 T cells inhibited Th1 and Th17 polarization, as well as the release of IFN-γ and IL-17 in the culture supernatant.: Our results show that a decreased TGR5 expression might contribute to the pathogenesis of VKH disease.
目的
探讨 G 蛋白偶联胆汁酸受体 1（Gpbar1，即 TGR5）在 Vogt-小柳原田综合征（VKH）发病机制中的作用。
方法
采用实时 PCR 法检测巨噬细胞中 TGR5、iNOS、Arg1、CD16 和 CD206 的 mRNA 水平，采用 ELISA 法检测细胞培养上清液中细胞因子的产生，采用流式细胞术检测 CD4 IFN-γ 和 CD4 IL-17 T 细胞的频率。
结果
与正常对照组相比，活动期 VKH 患者 M1 巨噬细胞中 TGR5 的表达降低。INT-777 刺激 M1 巨噬细胞可使炎症性 M1 向抗炎性 M2 巨噬细胞亚型转变。与 CD4 T 细胞共培养的巨噬细胞激活 TGR5 可抑制 Th1 和 Th17 极化，以及培养上清液中 IFN-γ 和 IL-17 的释放。
结论
我们的研究结果表明，TGR5 表达降低可能导致 VKH 病的发病机制。
Zotero 插件