小柯机器人

胃细菌诱导的2型先天淋巴样细胞通过IgA提供免疫保护
2020-04-02 17:13

2020年4月1日,《免疫》杂志在线发表了日本理化学研究所Hiroshi Ohno、Naoko Satoh-Takayama等研究人员的合作成果。他们的最新研究表明,胃细菌诱导的2型先天淋巴样细胞通过产生IgA来提供免疫保护。

研究人员发现,2型先天淋巴样细胞(ILC2)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局部共生菌群的调节。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的扩增和激活。幽门螺杆菌感染能够迅速诱导胃部的ILC2。ILC2来源的IL-5导致IgA产生,其可在无特定病原体(SPF)和幽门螺杆菌感染的小鼠中包裹胃细菌。因此,这项研究鉴定了由共生微生物调节的ILC2依赖性IgA反应,从而通过消除IgA包裹的细菌(包括病原性幽门螺杆菌)来保护胃。
 
据悉,肠道菌群能够在局部和全身改变并影响免疫系统的发育,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。 
 
附:英文原文

Title: Bacteria-Induced Group 2 Innate Lymphoid Cells in the Stomach Provide Immune Protection through Induction of IgA

Author: Naoko Satoh-Takayama, Tamotsu Kato, Yasutaka Motomura, Tomoko Kageyama, Naoko Taguchi-Atarashi, Ryo Kinoshita-Daitoku, Eisuke Kuroda, James P. Di Santo, Hitomi Mimuro, Kazuyo Moro, Hiroshi Ohno

Issue&Volume: 2020-04-01

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

DOI: 10.1016/j.immuni.2020.03.002

Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30090-X

Immunity:《免疫》,创刊于1994年。隶属于细胞出版社,最新IF:43.474
官方网址:https://www.cell.com/immunity/home
投稿链接:https://www.editorialmanager.com/immunity/default.aspx


本期文章:《免疫》:Online/在线发表

分享到:

0