| First Author | Qiu J | Year | 2012 |
| Journal | Immunity | Volume | 36 |
| Issue | 1 | Pages | 92-104 |
| PubMed ID | 22177117 | Mgi Jnum | J:180786 |
| Mgi Id | MGI:5307210 | Doi | 10.1016/j.immuni.2011.11.011 |
| Citation | Qiu J, et al. (2012) The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells. Immunity 36(1):92-104 |
| abstractText | Innate lymphoid cells (ILCs) expressing the nuclear receptor RORgammat are essential for gut immunity presumably through production of interleukin-22 (IL-22). The molecular mechanism underlying the development of RORgammat(+) ILCs is poorly understood. Here, we have shown that the aryl hydrocarbon receptor (Ahr) plays an essential role in RORgammat(+) ILC maintenance and function. Expression of Ahr in the hematopoietic compartment was important for accumulation of adult but not fetal intestinal RORgammat(+) ILCs. Without Ahr, RORgammat(+) ILCs had increased apoptosis and less production of IL-22. RORgammat interacted with Ahr and promoted Ahr binding at the Il22 locus. Upon IL-23 stimulation, Ahr-deficient RORgammat(+) 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 RORgammat(+) ILCs. |
