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- W1603640418 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." @default.
- W1603640418 created "2016-06-24" @default.
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- W1603640418 date "2010-09-15" @default.
- W1603640418 modified "2023-10-16" @default.
- W1603640418 title "An Interaction between Kynurenine and the Aryl Hydrocarbon Receptor Can Generate Regulatory T Cells" @default.
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- W1603640418 doi "https://doi.org/10.4049/jimmunol.0903670" @default.
- W1603640418 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2952546" @default.
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