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Cited by 859

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells

Open access
Qiu, Ju, Heller, Jennifer J., Guo, Xiaohuan, Chen, Zong-ming E., Fish, Kamonwan, Fu, Yang-Xin, Zhou, Liang·2012·Immunity

Abstract

SUMMARY Innate lymphoid cells (ILCs) expressing the nuclear receptor RORγt are essential for gut immunity presumably through production of interleukin (IL)-22. The molecular mechanism underlying the development of RORγt+ ILCs is poorly understood. Here, we have shown that the aryl hydrocarbon receptor (Ahr) plays an essential role in RORγt+ ILC maintenance and function. Expression of Ahr in the hematopoietic compartment was important for accumulation of adult but not fetal intestinal RORγt+ ILCs. Without Ahr, RORγt+ ILCs had increased apoptosis and less production of IL-22. RORγt interacted with Ahr and promoted Ahr binding at the Il22 locus. Upon IL-23 stimulation, Ahr-deficient RORγt+ ILCs had reduced IL-22 expression, consistent with downregulation of IL-23R in those cells. Ahr-deficient mice succumbed to Citrobacter rodentium infection, while 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 RORγt+ ILCs.

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Metadata

Authors
Qiu, J., Heller, J. J., Guo, X., Chen, Z.-M. E., Fish, K., Fu, Y.-X., & Zhou, L.
Venue
Immunity
Publisher
Elsevier BV
Published
2012-01
Volume
36
Issue
1
Pages
92-104
ISSN
1074-7613 (ISSN-L)
OpenAlex
W1981177186
Cited by
859
References
8
FWCI
16.44
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells. https://app.cochat.ai/papers/10.1016/j.immuni.2011.11.011
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Qiu, J., Heller, J. J., Guo, X., Chen, Z.-M. E., Fish, K., Fu, Y.-X., & Zhou, L. (2012). The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells. Immunity. https://doi.org/10.1016/j.immuni.2011.11.011

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