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J Immunol. 2010 Sep 15;185(6):3190-8. doi: 10.4049/jimmunol.0903670. Epub 2010 Aug 18.

An interaction between kynurenine and the aryl hydrocarbon receptor can generate regulatory T cells.

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  • 1Division of Transplantation, Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792-7375, USA. mezrich@surgery.wisc.edu

Abstract

The aryl hydrocarbon receptor (AHR) has been known to cause immunosuppression after binding dioxin. It has recently been discovered that the receptor may be central to T cell differentiation into FoxP3(+) regulatory T cells (Tregs) versus Th17 cells. In this paper, we demonstrate that kynurenine, the first breakdown product in the IDO-dependent tryptophan degradation pathway, activates the AHR. We furthermore show that this activation leads to AHR-dependent Treg generation. We additionally investigate the dependence of TGF-beta on the AHR for optimal Treg generation, which may be secondary to the upregulation of this receptor that is seen in T cells postexposure to TGF-beta. These results shed light on the relationship of IDO to the generation of Tregs, in addition to highlighting the central importance of the AHR in T cell differentiation. All tissues and cells were derived from mice.

PMID:
20720200
[PubMed - indexed for MEDLINE]
PMCID:
PMC2952546
Free PMC Article
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