Author Correction: Commensal microflora-induced T cell responses mediate progressive neurodegeneration in glaucoma.
Author Correction: Commensal microflora-induced T cell responses mediate progressive neurodegeneration in glaucoma.
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DOI：
10.1038/s41467-018-06428-2
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发表时间：
2018-09-20
影响因子：
16.6
通讯作者：
Chen DF
中科院分区：
文献类型：
--
作者：
Chen H;Cho KS;Vu THK;Shen CH;Kaur M;Chen G;Mathew R;McHam ML;Fazelat A;Lashkari K;Au NPB;Tse JKY;Li Y;Yu H;Yang L;Stein-Streilein J;Ma CHE;Woolf CJ;Whary MT;Jager MJ;Fox JG;Chen J;Chen DF
青光眼是世界上最常见的神经退行性疾病，也是致盲的主要原因。青光眼神经变性的发病机制尚不完全清楚。在这里，我们通过使用T细胞和/或B细胞缺乏和过继细胞移植的小鼠，发现眼压（IOP）的短暂升高足以诱导T细胞渗入视网膜。这种t细胞浸润导致视网膜神经节细胞变性期延长，这种变性在IOP恢复到正常水平后仍持续存在。热休克蛋白（HSP）是青光眼小鼠和人青光眼患者t细胞反应的靶抗原。此外，视网膜浸润性T细胞与人和细菌热休克蛋白发生交叉反应；在没有共生菌群的情况下饲养的小鼠不会出现青光眼t细胞反应或相关的神经变性。这些结果提供了令人信服的证据，证明青光眼神经变性部分是由暴露于共生菌群预致敏的T细胞介导的。
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.
影响因子：
16.6
作者：
Chen H;Cho KS;Vu THK;Shen CH;Kaur M;Chen G;Mathew R;McHam ML;Fazelat A;Lashkari K;Au NPB;Tse JKY;Li Y;Yu H;Yang L;Stein-Streilein J;Ma CHE;Woolf CJ;Whary MT;Jager MJ;Fox JG;Chen J;Chen DF
通讯作者：
Chen DF