Journal
IMMUNITY
Volume 36, Issue 1, Pages 92-104Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.11.011
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Funding
- National Institutes of Health [AI 089954, AI091962, CA141975, AI090392]
- Pew Scholarship
- Cancer Research Institute
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Innate lymphoid cells (ILCs) expressing the nuclear receptor ROR gamma t are essential for gut immunity presumably through production of interleukin-22 (IL-22). The molecular mechanism underlying the development of ROR gamma t(+) ILCs is poorly understood. Here, we have shown that the aryl hydrocarbon receptor (Ahr) plays an essential role in ROR gamma t(+) ILC maintenance and function. Expression of Ahr in the hematopoietic compartment was important for accumulation of adult but not fetal intestinal ROR gamma t(+) ILCs. Without Ahr, ROR gamma t(+) ILCs had increased apoptosis and less production of IL-22. ROR gamma t interacted with Ahr and promoted Ahr binding at the 1122 locus. Upon IL-23 stimulation, Ahr-deficient ROR gamma t(+) ILCs had reduced IL-22 expression, consistent with downregulation of IL-23R in those cells. Ahr-deficient mice succumbed to Citrobacter rodentium infection, whereas ectopic expression of IL-22 protected animals from early mortality. Our data uncover a previously unrecognized physiological role for Ahr in promoting innate gut immunity by regulating ROR gamma t(+) ILCs.
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