期刊
SCIENCE
卷 348, 期 6238, 页码 1031-1035出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaa4812
关键词
-
资金
- National Institutes of Health [DP5OD012116, DK071176]
- National Institute of Allergy and Infectious Diseases Mucosal Immunology Studies Team (MIST) Scholar Award in Mucosal Immunity
- Institute for Translational Medicine and Therapeutics Transdisciplinary Program in Translational Medicine and Therapeutics (from the U.S. National Center for Research Resources) [UL1-RR024134]
- Crohn's and Colitis Foundation of America (CCFA) [297365]
- Cancer Research Institute Student Training and Research in Tumor immunology (STaRT) grant
- Wellcome Trust Research Career Development Fellowship
Inflammatory CD4(+) T cell responses to self or commensal bacteria underlie the pathogenesis of autoimmunity and inflammatory bowel disease (IBD), respectively. Although selection of self-specific T cells in the thymus limits responses to mammalian tissue antigens, the mechanisms that control selection of commensal bacteria-specific T cells remain poorly understood. Here, we demonstrate that group 3 innate lymphoid cell (ILC3)-intrinsic expression of major histocompatibility complex class II (MHCII) is regulated similarly to thymic epithelial cells and that MHCII+ ILC3s directly induce cell death of activated commensal bacteria-specific T cells. Further, MHCII on colonic ILC3s was reduced in pediatric IBD patients. Collectively, these results define a selection pathway for commensal bacteria-specific CD4(+) T cells in the intestine and suggest that this process is dysregulated in human IBD.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据