A20 Inhibits Intraocular Inflammation in Mice by Regulating the Function of CD4+T Cells and RPE Cells.
A20 Inhibits Intraocular Inflammation in Mice by Regulating the Function of CD4+T Cells and RPE Cells.
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A20 通过调节 CD4 T 细胞和 RPE 细胞的功能抑制小鼠眼内炎症
DOI：
10.3389/fimmu.2020.603939
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发表时间：
2020
影响因子：
7.3
通讯作者：
Li H
中科院分区：
文献类型：
--
作者：
Hu J;Yi S;Wang C;Zhang Y;Tang J;Huang X;Yang L;Yang J;Li H
A20是炎症和免疫的负调节因子，在多种自身免疫性和炎症性疾病中发挥作用。在这里，我们证明A20过表达通过抑制Th 1和Th 17细胞的浸润以及保护血视网膜屏障的完整性来显著改善EAU的严重程度。体外研究表明，A20沉默可以促进CD 4 +T细胞向Th 1和Th 17表型发展。活动性BD患者CD 4 +T细胞A20表达降低，而VKH患者则无此现象。此外，A20基因沉默可诱导hRPE细胞产生IL-6、IL-8和MCP-1，并下调ZO-1和occludin的表达，这是通过抑制MAPK和NF-κB途径介导的。这项研究揭示了A20预防自身免疫性葡萄膜炎的机制。
A20 is a negative regulator of inflammation and immunity and plays a role in several autoimmune and inflammatory diseases. Here, we demonstrate that A20 overexpression significantly ameliorates severity of EAU by inhibiting the infiltration of Th1 and Th17 cells, and by protecting integrity of the blood retinal barrier. In vitro studies showed that A20 silencing could promote CD4+T cells toward a Th1 and Th17 phenotype. A decreased expression of A20 in CD4+T cells was noticed in active BD patients but not in VKH patients. Furthermore, silencing of A20 in hRPE cells induced the production of IL-6, IL-8, and MCP-1 and downregulated ZO-1 and occludin expression which is mediated by inhibition of MAPK and NF-κB pathways. This study reveals a mechanism by which A20 prevents autoimmune uveitis.
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影响因子：
4.9
作者：
Koczan D;Drynda S;Hecker M;Drynda A;Guthke R;Kekow J;Thiesen HJ
通讯作者：
Thiesen HJ
影响因子：
7.7
作者：
Boonyasrisawat, Watip;Eberle, Delphine;Doria, Alessandro
通讯作者：
Doria, Alessandro
影响因子：
20.3
作者：
Chu, Yuanyuan;Vahl, J. Christoph;Schmidt-Supprian, Marc
通讯作者：
Schmidt-Supprian, Marc
影响因子：
56.9
作者：
Lee, EG;Boone, DL;Ma, A
通讯作者：
Ma, A
DOI：
10.3109/01676830.2013.833253
发表时间：
2013-01-01
期刊：
ORBIT-AN INTERNATIONAL JOURNAL ON ORBITAL DISORDERS AND FACIAL RECONSTRUCTIVE SURGERY
影响因子：
--
作者：
Ho, Tsai-Hsuan;Lin, Muh-Chiou;Bee, Youn-Shen
通讯作者：
Bee, Youn-Shen