期刊
SCIENCE
卷 336, 期 6086, 页码 1321-1325出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1222551
关键词
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资金
- NIH [AI061570, AI087990, AI074878, AI083480, AI095466, AI095608, T32-AI007532, T32-AI055428, T32-RR007063, K08-DK093784, AI47619, P30 AI 045008]
- Burroughs Wellcome Fund Investigator in Pathogenesis of Infectious Disease Award
- Philadelphia VA Medical Research and Merit Review
- American Gastroenterological Association
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Program for Promotion of Basic and Applied Researches for Innovations in Bio-Oriented Industry
- Matthew J. Ryan Veterinary Hospital Pathology Lab, the National Institute of Diabetes and Digestive and Kidney Disease Center for the Molecular Studies in Digestive and Liver Disease Molecular Pathology and Imaging Core [P30DK50306]
- National Cancer Institute (NCI) Comprehensive Cancer Center [2-P30 CA016520]
- Grants-in-Aid for Scientific Research [23229004] Funding Source: KAKEN
The mammalian intestinal tract is colonized by trillions of beneficial commensal bacteria that are anatomically restricted to specific niches. However, the mechanisms that regulate anatomical containment remain unclear. Here, we show that interleukin-22 (IL-22)-producing innate lymphoid cells (ILCs) are present in intestinal tissues of healthy mammals. Depletion of ILCs resulted in peripheral dissemination of commensal bacteria and systemic inflammation, which was prevented by administration of IL-22. Disseminating bacteria were identified as Alcaligenes species originating from host lymphoid tissues. Alcaligenes was sufficient to promote systemic inflammation after ILC depletion in mice, and Alcaligenes-specific systemic immune responses were associated with Crohn's disease and progressive hepatitis C virus infection in patients. Collectively, these data indicate that ILCs regulate selective containment of lymphoid-resident bacteria to prevent systemic inflammation associated with chronic diseases.
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