B7-H1 (CD274) inhibits the development of herpetic stromal keratitis (HSK)
B7-H1 (CD274) inhibits the development of herpetic stromal keratitis (HSK)
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DOI：
10.1016/j.febslet.2005.09.098
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发表时间：
2005-11-07
期刊：
影响因子：
3.5
通讯作者：
Choi, IH
中科院分区：
文献类型：
--
作者：
Jun, H;Seo, SK;Choi, IH
共信号分子B7-H1（CD 274）通过程序性死亡-1（PD-1）受体作为共抑制剂，通过T细胞上尚未鉴定的受体作为共刺激剂。我们研究了内源性B7-H1在单纯疱疹病毒1型（HSV-1）引起的单纯疱疹性角膜基质炎（HSK）发病机制中的生理作用。小鼠角膜感染HSV-1后，引流淋巴结（dLN）和炎症角膜中CD 11b（+）巨噬细胞群中B7-H1表达上调。此外，HSV-1感染显著增加了dLN和炎症角膜中CD 4（+）T细胞上的PD-1表达。B7-H1单克隆抗体可诱导HSV特异性CD 4（+）T细胞增殖，分泌IFN-γ，抑制HSV特异性CD 4（+）T细胞凋亡，加重HSK。提示B7-H1可能参与了HSK的发生发展过程。(c)2005年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
The co-signaling molecule B7-H1 (CD274) functions as both a co-inhibitor through programmed death-1 (PD-1) receptor and a co-stimulator via an as-yet-unidentified receptor on T cells. We investigated the physiological role of endogenous B7-H1 in the pathogenesis of herpetic stromal keratitis (HSK) caused by herpes simplex virus type 1 (HSV-1). Following HSV-1 infection of the cornea of mice, B7-H1 expression was up-regulated in the CD11b(+) macrophage population in the draining lymph nodes (dLN) and in the inflamed cornea. In addition, HSV-1 infection significantly increased PD-1 expression on CD4(+) T cells in the dLN and inflamed cornea. The administration of antagonistic B7-H1 monoclonal antibody resulted in the proliferation of HSV-specific CD4(+) T cells that secreted interferon (INF)-gamma, and inhibited the apoptosis of HSV-specific CD4(+) T cells, which exaggerated HSK. These results strongly suggest that the B7-H1 may be involved in suppression of the development of HSK. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.