https://www.sciencedirect.com/science/article/pii/S0896841119300241?via%3Dihub
https://www.ncbi.nlm.nih.gov/pubmed/31005389?dopt=Abstract
CD30L/CD30 protects against psoriasiform skin inflammation by suppressing Th17-related cytokine production by Vγ4+ γδ T cells.
J Autoimmun. 2019 Apr 18;:
Authors: Yue D, You Y, Zhang X, Wang B, Wang X, Qi R, Yang F, Meng X, Yoshikai Y, Wang Y, Sun X
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.
PMID: 31005389 [PubMed – as supplied by publisher]
CD30L/CD30 protects against psoriasiform skin inflammation by suppressing Th17-related cytokine production by Vγ4+ γδ T cells.
PubMed:31005389
Last Update Posted: 04/22/19 06:03AM