CD30L/CD30 protects against psoriasiform skin inflammation by suppressing Th17-related cytokine production by Vγ4+ γδ T cells. (July 2019)

• Record Type: Journal Article
• Authors: Yue, Dan; You, Yong; Zhang, Xiaoqing; Wang, Biao; Wang, Xiao; Qi, Ruiqun; Yang, Fan; Meng, Xin; Yoshikai, Yasunobu; Wang, Yuanyuan; Sun, Xun
• Is Part Of: Journal of autoimmunity. Volume 101(2019)
• Page Start: 70
• Page End: 85
• Publication Date: 2019-07
• Subjects: Psoriasis -- CD30 ligand -- Vγ4+ γδ T cells -- IL-17A -- CCR6; Autoimmunity -- Periodicals; Autoimmune diseases -- Periodicals; Autoantibodies -- Periodicals; Autoimmune Diseases -- Periodicals; Auto-immunité -- Périodiques; Maladies auto-immunes -- Périodiques; Electronic journals; 616.978005
• DOI: 10.1016/j.jaut.2019.04.009
• Languages: English
• ISSNs: 0896-8411

Abstract

Abstract: Psoriasis is a common, autoimmune, chronic inflammatory skin disease. It has been demonstrated that cutaneous T17 cells play an important pro-inflammatory role in the pathogenesis of psoriasis, through the production of various Th17-related cytokines. Our previous studies have demonstrated that CD30L/CD30 signal plays a pivotal role in the differentiation of CD4 + Th17 cells and Vγ6 + γδ T17 cells in the gut-associated lymphoid tissues of mouse. However, its effect on the pathogenesis of psoriasis is unknown. Here, we fully prove that CD30L/CD30 signaling plays a novel protective role in the development of psoriasis in mice, through selective inhibition of CCR6 expression and Th17-related cytokine synthesis in the Vγ4 + γδ T17 cell subset. Meanwhile, treatment with agonistic anti-CD30 mAb had a significant therapeutic effect on our psoriasis mouse model. Therefore, the CD30L/CD30 signaling pathway is an ideal target for antibody therapy, which may become a new approach for the immunobiological treatment of psoriasis.