Suppr超能文献

共生微生物诱导的 T 细胞反应介导青光眼的进行性神经退行性变。

Commensal microflora-induced T cell responses mediate progressive neurodegeneration in glaucoma.

机构信息

Department of Ophthalmology, Second Xiangya Hospital of Central South University Changsha, Hunan Province, 410011, Hunan, China.

Institution of Ophthalmic Center, Changsha, Hunan Province, 410011, Hunan, China.

出版信息

Nat Commun. 2018 Aug 10;9(1):3209. doi: 10.1038/s41467-018-05681-9.

Abstract

Glaucoma is the most prevalent neurodegenerative disease and a leading cause of blindness worldwide. The mechanisms causing glaucomatous neurodegeneration are not fully understood. Here we show, using mice deficient in T and/or B cells and adoptive cell transfer, that transient elevation of intraocular pressure (IOP) is sufficient to induce T-cell infiltration into the retina. This T-cell infiltration leads to a prolonged phase of retinal ganglion cell degeneration that persists after IOP returns to a normal level. Heat shock proteins (HSP) are identified as target antigens of T-cell responses in glaucomatous mice and human glaucoma patients. Furthermore, retina-infiltrating T cells cross-react with human and bacterial HSPs; mice raised in the absence of commensal microflora do not develop glaucomatous T-cell responses or the associated neurodegeneration. These results provide compelling evidence that glaucomatous neurodegeneration is mediated in part by T cells that are pre-sensitized by exposure to commensal microflora.

摘要

青光眼是最常见的神经退行性疾病,也是全球导致失明的主要原因。导致青光眼神经退行性变的机制尚未完全阐明。在这里,我们使用缺乏 T 细胞和/或 B 细胞的小鼠和过继细胞转移,表明眼内压(IOP)的短暂升高足以诱导 T 细胞浸润到视网膜。这种 T 细胞浸润导致视网膜神经节细胞变性的延长阶段,即使 IOP 恢复到正常水平后仍持续存在。热休克蛋白(HSP)被鉴定为青光眼小鼠和人类青光眼患者 T 细胞反应的靶抗原。此外,浸润到视网膜的 T 细胞与人类和细菌 HSP 发生交叉反应;在缺乏共生微生物群的情况下饲养的小鼠不会产生青光眼 T 细胞反应或相关的神经退行性变。这些结果提供了令人信服的证据,表明青光眼神经退行性变部分是由预先致敏于共生微生物群的 T 细胞介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11a5/6086830/aeef182e0fd5/41467_2018_5681_Fig1_HTML.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验