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IL-23 promotes TCR-mediated negative selection of thymocytes through the upregulation of IL-23 receptor and RORγt

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Listed:
  • Hao Li

    (University of Alabama at Birmingham
    University of Alabama at Birmingham)

  • Hui-Chen Hsu

    (University of Alabama at Birmingham)

  • Qi Wu

    (University of Alabama at Birmingham)

  • PingAr Yang

    (University of Alabama at Birmingham)

  • Jun Li

    (University of Alabama at Birmingham)

  • Bao Luo

    (University of Alabama at Birmingham)

  • Mohamed Oukka

    (University of Washington)

  • Claude H. Steele

    (Allergy & Critical Care, University of Alabama at Birmingham)

  • Daniel J. Cua

    (Merck Research Laboratories)

  • William E. Grizzle

    (Clinical Pathology & Anatomic Pathology, University of Alabama at Birmingham)

  • John D. Mountz

    (University of Alabama at Birmingham
    Birmingham VA Medical Center)

Abstract

Transient thymic involution is frequently found during inflammation, yet the mode of action of inflammatory cytokines is not well defined. Here we report that interleukin-23 (IL-23) production by the thymic dendritic cells (DCs) promotes apoptosis of the CD4hiCD8hi double-positive (DP) thymocytes. A deficiency in IL-23 signalling interferes with negative selection in the male Db/H-Y T-cell receptor (TCR) transgenic mice. IL-23 plus TCR signalling results in significant upregulation of IL-23 receptor (IL-23R) expressed predominantly on CD4hiCD8hiCD3+αβTCR+ DP thymocytes, and leads to RORγt-dependent apoptosis. These results extend the action of IL-23 beyond its peripheral effects to a unique role in TCR-mediated negative selection including elimination of natural T regulatory cells in the thymus.

Suggested Citation

  • Hao Li & Hui-Chen Hsu & Qi Wu & PingAr Yang & Jun Li & Bao Luo & Mohamed Oukka & Claude H. Steele & Daniel J. Cua & William E. Grizzle & John D. Mountz, 2014. "IL-23 promotes TCR-mediated negative selection of thymocytes through the upregulation of IL-23 receptor and RORγt," Nature Communications, Nature, vol. 5(1), pages 1-13, September.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5259
    DOI: 10.1038/ncomms5259
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