γ-Tocotrienol inhibits T helper 17 cell differentiation via the IL-6/JAK/STAT3 signaling pathway

被引:5
|
作者
Zhao, Hanqing [1 ]
Guo, Xin [1 ]
Lei, Yunxuan [1 ]
Xia, Wenjie [2 ]
Cai, Feiyang [1 ]
Zhu, Dehao [1 ,3 ]
An, Yang [1 ]
Xi, Yebin [1 ]
Niu, Xiaoyin [1 ]
Wang, Zhaojun [1 ]
Yue, Tao [2 ]
Chen, Guangjie [1 ]
机构
[1] Shanghai Jiao Tong Univ, Shanghai Inst Immunol, Sch Med, Dept Immunol & Microbiol, Shanghai 200025, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Guanghua Hosp, Dept Rheumatol, Shanghai 200052, Peoples R China
[3] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Rheumatol & Immunol, Shanghai 200025, Peoples R China
关键词
-Tocotrienol; T helper 17 cells; JAK-STAT pathway; Cell differentiation; Psoriasis; VITAMIN-E; PATHOGENESIS; PSORIASIS; T(H)17;
D O I
10.1016/j.molimm.2022.09.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
gamma-Tocotrienol (GT3), a member of the vitamin E family, is well known for its medicinal value in clinical treat-ments. However, the role of GT3 in T helper 17 (Th17)/regulatory T cell (Treg) differentiation and function is not fully understood. Here, we demonstrated that GT3 suppressed Th17 differentiation in vitro by inhibiting signal transducer and activator of transcription 3 (STAT3) phosphorylation in the interleukin 6 (IL-6)/Janus kinase (JAK)/STAT3 signaling pathway. GT3 also inhibited HIF1A expression in Th17 metabolism. Additionally, we showed that GT3 treatment inhibited disease aggravation in an imiquimod (IMQ)-induced psoriasis-like mouse model by reducing the percentage of Th17 cells in the spleen in vivo. The findings of this study demonstrated the effects of GT3 on Th17 cells through the STAT3 signaling pathway.
引用
收藏
页码:126 / 133
页数:8
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