The prostaglandin E2 increases the production of IL-17 and the expression of costimulatory molecules on γδ T cells in rheumatoid arthritis

被引:12
作者
Du, Boyu [1 ,2 ]
Zhu, Min [1 ]
Li, Youling [3 ]
Li, Gang [3 ]
Xi, Xueyan [1 ,3 ,4 ]
机构
[1] Hubei Univ Med, Inst Basic Med Sci, Shiyan, Peoples R China
[2] Hubei Univ Med, Hubei Key Lab Wudang Local Chinese Med Res, Shiyan, Peoples R China
[3] Hubei Univ Med, Renmin Hosp, Shiyan, Peoples R China
[4] Hubei Univ Med, Hubei Key Lab Embryon Stem Cell Res, Shiyan, Peoples R China
基金
中国国家自然科学基金;
关键词
antigen presenting; IL-17; rheumatoid arthritis; gamma delta T cells; COLLAGEN-INDUCED ARTHRITIS; TUMOR-NECROSIS-FACTOR; ANTIGEN; TCR;
D O I
10.1111/sji.12872
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
gamma delta T cells play important roles in the development of rheumatoid arthritis (RA) through their antigen-presenting capacity, release of pro-inflammatory cytokines, immunomodulatory properties, interaction with CD4(+)CD25(+) Tregs and promotion of antibody production by helping B cells. Although prostaglandin E2 (PGE2) was proved to have the ability to enhance the antigen-presenting function of dendritic cells and IL-17 production of CD4(+) alpha beta T cells in RA, the role of PGE2 in gamma delta T cells from RA disease has not yet been clarified. The goal of this study was to determine the role of PGE2 in gamma delta T cells in RA. We first demonstrated that the population of gamma delta T17 cells increased in patients with RA compared to healthy controls. Then, IL-17A level in patients with RA was shown to increase compared to healthy controls. After adding PGE2 to gamma delta T cells from patients with RA, the IL-17A level increased accordingly, and the expression of the costimulatory molecules, CD80 and CD86, on these cells also increased. These results suggest that PEG2 can increase the production of IL-17A and the expression of CD80 and CD86 on gamma delta T cells in patients with RA. These findings will benefit to explore new therapeutic targets for RA disease.
引用
收藏
页数:7
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