Journal
CELL REPORTS
Volume 23, Issue 13, Pages 3750-3758Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.05.099
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Funding
- Japan Society for the Promotion of Science Overseas Research Fellowships
- German Research Foundation [KL 2963/1-1]
- Novo Nordic Foundation [14052]
- Jill Roberts Institute
- Wellcome Trust [110199/Z/15/Z]
- Crohn's and Colitis Foundation of America
- Searle Scholars Program
- American Asthma Foundation Scholar Award
- Burroughs Wellcome Fund
- NIH [DP5OD012116, AI123368, DK110262, AI095608, AI074878, AI083480, AI095466, AI102942, AI097333, AI106697]
- Wellcome Trust [110199/Z/15/Z] Funding Source: Wellcome Trust
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The intestinal tract is constantly exposed to various stimuli. Group 3 innate lymphoid cells (ILC3s) reside in lymphoid organs and in the intestinal tract and are required for immunity to enteric bacterial infection. However, the mechanisms that regulate the ILC3s in vivo remain incompletely defined. Here, we show that GPR183, a chemotactic receptor expressed on murine and human ILC3s, regulates ILC3 migration toward its ligand 7 alpha,25-dihydroxycholesterol (7 alpha,25-OHC) in vitro, and GPR183 deficiency in vivo leads to a disorganized distribution of ILC3s in mesenteric lymph nodes and decreased ILC3 accumulation in the intestine. GPR183 functions intrinsically in ILC3s, and GPR183-deficient mice are more susceptible to enteric bacterial infection. Together, these results reveal a role for the GPR183-7 alpha,25-OHC pathway in regulating the accumulation, distribution, and anti-microbial and tissue-protective functions of ILC3s and define a critical role for this pathway in promoting innate immunity to enteric bacterial infection.
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