The intestinal microbiota shapes and directs immune development locally and systemically, but little is known about whether commensal microbes in the stomach can impact their immunological microenvironment. Here, we report that group 2 innate lymphoid cells (ILC2s) were the predominant ILC subset in the stomach and show that their homeostasis and effector functions were regulated by local commensal communities. Microbes elicited interleukin-7 (IL-7) and IL-33 production in the stomach, which in turn triggered the propagation and activation of ILC2. Stomach ILC2s were also rapidly induced following infection with Helicobacter pylori. ILC2-derived IL-5 resulted in the production of IgA, which coated stomach bacteria in both specific pathogen-free (SPF) and H. pylori-infected mice. Our study thus identifies ILC2-dependent IgA response that is regulated by the commensal microbiota, which is implicated in stomach protection by eliminating IgA-coated bacteria including pathogenic H. pylori.

肠道菌群在局部和全身形成并指导免疫系统的发展，但是人们对胃中的共生微生物是否会影响其免疫微环境知之甚少。在这里，我们报告第2组先天淋巴样细胞（ILC2s）是胃中主要的ILC亚型，并表明它们的稳态和效应子功能受到当地共生社区的调节。微生物在胃中引起白介素7（IL-7）和IL-33的产生，进而触发了ILC2的传播和激活。幽门螺杆菌感染后还可迅速诱导胃ILC2s 。源自ILC2的IL-5导致IgA的产生，它以无特定病原体（SPF）和幽门螺杆菌的形式包被胃细菌感染的小鼠。因此，我们的研究确定了由共生菌群调节的依赖ILC2的IgA反应，这是通过消除包括病原性幽门螺杆菌的IgA包被的细菌参与胃保护。