Differential developmental requirement and peripheral regulation for dermal Vγ4 and Vγ6T17 cells in health and inflammation

Yihua Cai, Feng Xue, Chris Fleming, Jie Yang, Chuanlin Ding, Yunfeng Ma, Min Liu, Huang-ge Zhang, Jie Zheng, Na Xiong and Jun Yan ()
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Yihua Cai: James Graham Brown Cancer Center, University of Louisville
Feng Xue: Ruijin Hospital, School of Medicine, Shanghai Jiaotong University
Chris Fleming: James Graham Brown Cancer Center, University of Louisville
Jie Yang: Pennsylvania State University
Chuanlin Ding: James Graham Brown Cancer Center, University of Louisville
Yunfeng Ma: James Graham Brown Cancer Center, University of Louisville
Min Liu: James Graham Brown Cancer Center, University of Louisville
Huang-ge Zhang: James Graham Brown Cancer Center, University of Louisville
Jie Zheng: Ruijin Hospital, School of Medicine, Shanghai Jiaotong University
Na Xiong: Pennsylvania State University
Jun Yan: James Graham Brown Cancer Center, University of Louisville

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract Dermal IL-17-producing γδT cells have a critical role in skin inflammation. However, their development and peripheral regulation have not been fully elucidated. Here we demonstrate that dermal γδT cells develop from the embryonic thymus and undergo homeostatic proliferation after birth with diversified TCR repertoire. Vγ6T cells are bona fide resident, but precursors of dermal Vγ4T cells may require extrathymic environment for imprinting skin-homing properties. Thymic Vγ6T cells are more competitive than Vγ4 for dermal γδT cell reconstitution and TCRδ−/− mice reconstituted with Vγ6 develop psoriasis-like inflammation after IMQ-application. Although both IL-23 and IL-1β promote Vγ4 and Vγ6 proliferation, Vγ4 are the main source of IL-17 production that requires IL-1 signalling. Mice with deficiency of IL-1RI signalling have significantly decreased skin inflammation. These studies reveal a differential developmental requirement and peripheral regulation for dermal Vγ6 and Vγ4 γδT cells, implying a new mechanism that may be involved in skin inflammation.

Date: 2014
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DOI: 10.1038/ncomms4986

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