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An Interaction between Kynurenine and the Aryl Hydrocarbon Receptor Can Generate Regulatory T Cells

Joshua D. Mezrich, John H. Fechner, Xiaoji Zhang, Brian P. Johnson, William J. Burlingham and Christopher A. Bradfield
J Immunol September 15, 2010, 185 (6) 3190-3198; DOI: https://doi.org/10.4049/jimmunol.0903670
Joshua D. Mezrich
*Division of Transplantation, Department of Surgery and
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John H. Fechner
*Division of Transplantation, Department of Surgery and
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Xiaoji Zhang
*Division of Transplantation, Department of Surgery and
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Brian P. Johnson
†McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792
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William J. Burlingham
*Division of Transplantation, Department of Surgery and
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Christopher A. Bradfield
†McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792
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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-β 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-β. 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.

Footnotes

  • This work was supported by Grant 1UL1RR025011 from the Clinical and Translational Science Award program of the National Center for Research Resources, National Institutes of Health (to J.D.M.), National Institute on Environmental Health Sciences Grant R37ES005703 (to C.A.B.), National Cancer Institute Grant P30CA014520 (to C.A.B.), an American Society of Transplant Surgeons-Astellas Faculty Development Award (to J.D.M.), National Institute of Allergy and Infectious Diseases Grant RO1AI066219 (to W.J.B.), and National Institutes of Health Training Grant T32ES007015-32 (to B.P.J.).

  • The online version of this article contains supplemental material.

  • Abbreviations used in this paper:

    AHR
    aryl hydrocarbon receptor
    BMDC
    bone marrow-derived dendritic cell
    DC
    dendritic cell
    DRE
    dioxin-responsive element
    FICZ
    6-formylindolo[3,2-b]carbazole
    nt
    not tested
    pDC
    plasmacytoid dendritic cell
    qPCR
    quantitative PCR
    TCDD
    2,3,7,8-tetrachlorodibenzo-p-dioxin
    Treg
    regulatory T cell
    WT
    wild-type.

  • Received November 13, 2009.
  • Accepted July 8, 2010.
  • Copyright © 2010 by The American Association of Immunologists, Inc.
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The Journal of Immunology: 185 (6)
The Journal of Immunology
Vol. 185, Issue 6
15 Sep 2010
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An Interaction between Kynurenine and the Aryl Hydrocarbon Receptor Can Generate Regulatory T Cells
Joshua D. Mezrich, John H. Fechner, Xiaoji Zhang, Brian P. Johnson, William J. Burlingham, Christopher A. Bradfield
The Journal of Immunology September 15, 2010, 185 (6) 3190-3198; DOI: 10.4049/jimmunol.0903670

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An Interaction between Kynurenine and the Aryl Hydrocarbon Receptor Can Generate Regulatory T Cells
Joshua D. Mezrich, John H. Fechner, Xiaoji Zhang, Brian P. Johnson, William J. Burlingham, Christopher A. Bradfield
The Journal of Immunology September 15, 2010, 185 (6) 3190-3198; DOI: 10.4049/jimmunol.0903670
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