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

Hao Li, Hui-Chen Hsu (), Qi Wu, PingAr Yang, Jun Li, Bao Luo, Mohamed Oukka, Claude H. Steele, Daniel J. Cua, William E. Grizzle and John D. Mountz ()
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Hao Li: 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

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms5259

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