Abstract：
How group 3 innate lymphoid cells (ILC3s) regulate mucosal protection in the presence of T cells remains poorly understood. Here, we examined ILC3 function in intestinal immunity using ILC3-deficient mice that maintain endogenous T cells, T helper 17 (TH17) cells, and secondary lymphoid organs. ILC3s were dispensable for generation of TH17 and TH22 cell responses to commensal and pathogenic bacteria, and absence of ILC3s did not affect IL-22 production by CD4 T cells before or during infection. However, despite the presence of IL-22-producing T cells, ILC3s and ILC3-derived IL-22 were required for maintaining homeostatic functions of the intestinal epithelium. T cell-sufficient, ILC3-deficient mice were capable of pathogen clearance and survived infection with a low dose of Citrobacter rodentium. However, ILC3s promoted pathogen tolerance at early time points of infection by activating tissue-protective immune pathways. Consequently, ILC3s were indispensable for survival after high-dose infection. Our results demonstrate a context-dependent role for ILC3s in immune-sufficient animals and provide a blueprint for uncoupling of ILC3 and TH17 cell functions.
摘要：
第3组先天淋巴样细胞（ILC3s）如何在T细胞存在下调节粘膜保护仍然知之甚少。这里,我们使用维持内源性T细胞的ILC3缺陷小鼠检查了ILC3在肠道免疫中的功能，辅助性T细胞17(TH17),和次级淋巴器官.ILC3对于产生对共生细菌和病原菌的TH17和TH22细胞反应是可有可无的，在感染之前或期间，ILC3的缺失不会影响CD4T细胞产生IL-22。然而,尽管存在产生IL-22的T细胞，ILC3和ILC3衍生的IL-22是维持肠上皮稳态功能所必需的。T细胞充足，ILC3缺陷型小鼠能够清除病原体，并在低剂量的柠檬酸杆菌啮齿动物感染下存活。然而,ILC3通过激活组织保护性免疫途径促进感染早期时间点的病原体耐受性。因此,ILC3对于高剂量感染后的生存是必不可少的。我们的结果证明了ILC3在免疫充足的动物中的环境依赖性作用，并为ILC3和TH17细胞功能的解偶联提供了蓝图。
