|開催日時：||2019年3月26日 16：00 ～ 17：00|
|演題：||Stomach ILC2s are regulated by commensal bacteria and can be activated in response to the pathobiont Helicobacter pylori.|
Innate lymphoid cells (ILCs) are composed of 3 different groups as ILC1s, ILC2s and ILC3s, which are divided based on the function and cell-development. ILCs are implicated as key initiators of immune responses at many organs including mucosal sites through their production of cytokines. Recent studies revealed that cytokines derived from ILC subsets can be triggered for the induction of diseases or disrupting homeostasis. The gut microbiota has a well-documented impact on immune development and regulation of immune responses, whereas the importance of microbiota for the ILCs-regulation in the mucosal tissues has not been well understood. Especially, very little is known about host microbial interactions, including immunological regulation and responses, in the stomach. We therefore compared two mucosal organs, small intestine (SI) and stomach, by focusing on ILC subsets from SPF and germ free (GF) mice. Different from the SI having distinct populations of ILC1s, ILC2s and ILC3s, the stomach had a large proportion of ILC2s with few ILC1s and virtually no ILC3s in SPF mice. These ILC2s are markedly decreased in GF compared to SPF mice. We found that microbes can elicit IL-7 and IL-33 production in the stomach, which in turn triggers ILC2s. We further detected that stomach ILC2s are also rapidly induced following infection with Helicobacter pylori (H. pylori), which in turn induced IgA production through IL-5 secretion. ILC2s in the stomach were still left unexamined especially in terms of relationship with microbes and innate immune responses. Our study thus identified a novel ILC2-dependent IgA response that is regulated by commensal and pathogenic bacteria, and implicated in barrier function in the stomach.
|世話人：||〇藤橋 浩太郎 （臨床ワクチン学分野）
植松 智 （自然免疫制御分野）