小柯机器人

美国国立卫生研究院Yasmine Belkaid团队的研究显示，内源性逆转录病毒调控体内微生物群的稳态和炎症反应。2021年6月23日，国际学术期刊《细胞》在线发表了这一成果。

研究人员发现皮肤微生物群促进了内源性逆转录病毒(ERV)的离散表达。角质形成细胞对ERV的内在反应取决于环GMP-AMP合酶(cGAS)/干扰素基因蛋白 (STING) 信号的刺激，并促进了共生特异性T细胞的产生。抑制ERV的逆转录显著影响了这些反应，导致对微生物群及其相关组织修复功能的免疫受损。相反，高脂质饮食会使的皮肤为响应共生ERV 的高表达做好准备，从而导致免疫反应和组织炎症增加。

总之，该结果支持以下观点，即宿主可能已经选择了其内源性病毒组作为与外源性微生物群进行交流的手段，从而产生了控制组织稳态和炎症的多界交流。 

据介绍，微生物群在调节宿主免疫方面发挥重要作用。然而，在很大程度上对微生物群免疫的启动和调节机制仍然未知。

附：英文原文

Title: Endogenous retroviruses promote homeostatic and inflammatory responses to the microbiota

Author: Djalma S. Lima-Junior, Siddharth R. Krishnamurthy, Nicolas Bouladoux, Nicholas Collins, Seong-Ji Han, Erin Y. Chen, Michael G. Constantinides, Verena M. Link, Ai Ing Lim, Michel Enamorado, Christophe Cataisson, Louis Gil, Indira Rao, Taylor K. Farley, Galina Koroleva, Jan Attig, Stuart H. Yuspa, Michael A. Fischbach, George Kassiotis, Yasmine Belkaid

Issue&Volume: 2021-06-23

Abstract: The microbiota plays a fundamental role in regulating host immunity. However, theprocesses involved in the initiation and regulation of immunity to the microbiotaremain largely unknown. Here, we show that the skin microbiota promotes the discreteexpression of defined endogenous retroviruses (ERVs). Keratinocyte-intrinsic responsesto ERVs depended on cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genesprotein (STING) signaling and promoted the induction of commensal-specific T cells.Inhibition of ERV reverse transcription significantly impacted these responses, resultingin impaired immunity to the microbiota and its associated tissue repair function.Conversely, a lipid-enriched diet primed the skin for heightened ERV- expression inresponse to commensal colonization, leading to increased immune responses and tissueinflammation. Together, our results support the idea that the host may have co-optedits endogenous virome as a means to communicate with the exogenous microbiota, resultingin a multi-kingdom dialog that controls both tissue homeostasis and inflammation.

DOI: 10.1016/j.cell.2021.05.020

Source: https://www.cell.com/cell/fulltext/S0092-8674(21)00650-4