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Innate lymphoid cells promote anatomical containment of lymphoid-resident commensal bacteria.

TitleInnate lymphoid cells promote anatomical containment of lymphoid-resident commensal bacteria.
Publication TypeJournal Article
Year of Publication2012
AuthorsSonnenberg GF, Monticelli LA, Alenghat T, Fung TC, Hutnick NA, Kunisawa J, Shibata N, Grunberg S, Sinha R, Zahm AM, Tardif MR, Sathaliyawala T, Kubota M, Farber DL, Collman RG, Shaked A, Fouser LA, Weiner DB, Tessier PA, Friedman JR, Kiyono H, Bushman FD, Chang K-M, Artis D
JournalScience
Volume336
Issue6086
Pagination1321-5
Date Published2012 Jun 8
ISSN1095-9203
KeywordsAdult, Alcaligenes, Animals, Bacterial Translocation, Crohn Disease, Hepatitis C, Chronic, Humans, Immunity, Innate, Inflammation, Interleukins, Intestines, Leukocyte L1 Antigen Complex, Liver, Lymph Nodes, Lymphocytes, Lymphoid Tissue, Macaca mulatta, Mice, Mice, Inbred C57BL, Middle Aged, Spleen, Young Adult
Abstract

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.

DOI10.1126/science.1222551
Alternate JournalScience
PubMed ID22674331
PubMed Central IDPMC3659421
Grant List2-P30 CA016520 / CA / NCI NIH HHS / United States
AI061570 / AI / NIAID NIH HHS / United States
AI074878 / AI / NIAID NIH HHS / United States
AI083480 / AI / NIAID NIH HHS / United States
AI087990 / AI / NIAID NIH HHS / United States
AI095466 / AI / NIAID NIH HHS / United States
AI095608 / AI / NIAID NIH HHS / United States
AI47619 / AI / NIAID NIH HHS / United States
K08 DK093784 / DK / NIDDK NIH HHS / United States
K08-DK093784 / DK / NIDDK NIH HHS / United States
P30 AI 045008 / AI / NIAID NIH HHS / United States
P30DK50306 / DK / NIDDK NIH HHS / United States
R01 AI061570 / AI / NIAID NIH HHS / United States
R01 AI074878 / AI / NIAID NIH HHS / United States
R01 AI095466 / AI / NIAID NIH HHS / United States
R01 AI102942 / AI / NIAID NIH HHS / United States
R21 AI083480 / AI / NIAID NIH HHS / United States
R21 AI087990 / AI / NIAID NIH HHS / United States
T32 AI007532 / AI / NIAID NIH HHS / United States
T32 RR007063 / RR / NCRR NIH HHS / United States
T32-AI007532 / AI / NIAID NIH HHS / United States
T32-AI055428 / AI / NIAID NIH HHS / United States
T32-RR007063 / RR / NCRR NIH HHS / United States
U01 AI095608 / AI / NIAID NIH HHS / United States

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