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Basic science

Aryl hydrocarbon receptor helps innate lymphoid cells control intestinal inflammation

▸ Qiu J, Guo X, Chen ZM, et al. Group 3 innate lymphoid cells inhibit T-cell-mediated intestinal inflammation through aryl hydrocarbon receptor signaling and regulation of microflora. Immunity 2013;39:386–99.

T helper (Th)17 cells, major producers of interleukin (IL)-17A, IL-17F and IL-22, are abundant in animal models of colitis and have been recovered from intestinal lesions of patients with IBD. RAR-related orphan receptor (RORγt)+ group 3 innate lymphoid cells (ILCs), which are important in gut immunity, exhibit a cytokine profile that resembles Th17 cells. The aryl hydrocarbon receptor (Ahr), a ligand-dependent transcription factor, is expressed by both intestinal Th17 cells and group 3 ILCs and promotes in vitro Th17 differentiation. Whether Ahr plays a role in the regulation of in vivo Th17 cell responses, especially in the gut, remains to be determined. In this study, the authors set out to investigate the role of Ahr in regulating Th17 cells in vivo using Ahr-deficient mice. Unexpectedly, the absence of Ahr led to an upregulation of IL-17 and downregulation of IL-22 by intestinal lymphocytes. Segmented filamentous bacteria (SFB), a type of intestinal commensal found in mice, have been shown to be important for in vivo Th17 induction. Antibiotic treatment decreased IL-17 production in the intestine indicating that uncontrolled expansion of SFB in Ahr-deficient mice contributes to increased Th17 cell responses in the gut. SFB growth and intestinal pathogenic Th17 responses in Ahr-deficient mice were due to a reduction in IL-22. In a T cell transfer model of colitis, ILCs played a protective role in controlling SFB and Th17 cell responses in the gut. Mice lacking Ahr and having a haplodeficiency of RORγt developed spontaneous colitis that was caused by innate deficiency of Ahr and dependent on gut flora. Collectively, this study describes a regulatory role for ILCs in controlling Th17 …

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  • Competing interests None.

  • Provenance and peer review Not commissioned; internally peer reviewed.