银屑病
CD14型
T细胞
炎症
单核细胞
细胞生物学
细胞
免疫学
细胞生长
化学
生物
癌症研究
医学
免疫系统
生物化学
作者
Jing Zhou,Jingjing Zhang,Tianlan Lu,Kexin Peng,Qiaoan Zhang,Kexiang Yan,Jing Luan,Jiewen Pan,Xiaohui Su,Jiping Sun,Zhenghua Zhang,Lei Shen
标识
DOI:10.1073/pnas.2117523119
摘要
Vγ9Vδ2 T cells play an important role in the development and progression of psoriasis vulgaris (PV), but how they promote skin inflammation and the molecular mechanisms underlying Vγ9Vδ2 T cell dysfunction are poorly understood. Here, we show that circulating Vγ9Vδ2 T cells are decreased and exhibit enhanced proliferation and increased production of IFN-γ and TNF-α in PV patients. Monocytes from PV patients express higher levels of the phosphoantigen sensor butyrophilin 3A1 (BTN3A1) than monocytes from healthy controls. Blockade of BTN3A1 suppresses Vγ9Vδ2 T cell activation and abolishes the difference in Vγ9Vδ2 T cell activation between PV patients and healthy controls. The CD14+ cells in PV skin lesions highly express BTN3A1 and juxtapose to Vδ2 T cells. In addition, IFN-γ induces the up-regulation of BTN3A1 on monocytes. Collectively, our results demonstrate a crucial role of BTN3A1 on monocytes in regulating Vγ9Vδ2 T cell activation and highlight BTN3A1 as a potential therapeutic target for psoriasis.
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