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SUMMARY: 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 Il22 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.

(C) 2012Elsevier, Inc.