Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608.
Department of Chemical and Biological Engineering, Northwestern University, Evanston, IL 60208.
Proc Natl Acad Sci U S A. 2019 Dec 3;116(49):24760-24769. doi: 10.1073/pnas.1908128116. Epub 2019 Nov 18.
Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identified opposing effects on ILCs by two species, and , isolated from immunocompromised mice. We demonstrated that the introduction of both species activated ILCs and induced gut inflammation; however, these species negatively regulated RORγt group 3 ILCs (ILC3s), especially T-bet ILC3s, and diminished their proliferative capacity. Thus, these findings underscore a previously unknown dichotomous regulation of ILC3s by species, and may serve as a model for further investigations to elucidate the host-microbe interactions that critically sustain the maintenance of intestinal ILC3s.
肠道固有淋巴细胞（ILCs）有助于肠道的保护性免疫和稳态，微生物群在塑造 ILC 功能方面起着至关重要的作用。然而，肠道微生物群在调节 ILC 的发育和维持中的作用仍然难以捉摸。在这里，我们鉴定了两种从免疫功能低下的小鼠中分离出来的细菌 和 对 ILCs 的相反作用。我们证明，这两种细菌的引入均激活了 ILCs 并诱导了肠道炎症；然而，这些细菌负调节 RORγt 组 3 ILC（ILC3），特别是 T-bet ILC3，并降低了它们的增殖能力。因此，这些发现强调了细菌对 ILC3 的一种以前未知的二分调节，并可能作为进一步研究的模型，以阐明对维持肠道 ILC3 的至关重要的宿主-微生物相互作用。
