Premium
The prostaglandin E2 increases the production of IL‐17 and the expression of costimulatory molecules on γδ T cells in rheumatoid arthritis
Author(s) -
Du Boyu,
Zhu Min,
Li Youling,
Li Gang,
Xi Xueyan
Publication year - 2020
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12872
Subject(s) - cd80 , cd86 , immunology , il 2 receptor , rheumatoid arthritis , medicine , prostaglandin e2 , antigen , antigen presenting cell , cd40 , t cell , biology , immune system , cytotoxic t cell , in vitro , biochemistry
γδ 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 + αβ T cells in RA, the role of PGE2 in γδ T cells from RA disease has not yet been clarified. The goal of this study was to determine the role of PGE2 in γδ T cells in RA. We first demonstrated that the population of γδT17 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 γδ 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 γδ T cells in patients with RA. These findings will benefit to explore new therapeutic targets for RA disease.