IL-17-producing gamma delta T cells are regulated by estrogen during development of experimental arthritis

摘要

Interleukin-17 (IL-17) drives inflammation and destruction of joints in rheumatoid arthritis (RA). The female sex hormone 17 beta-estradiol (E2) inhibits experimental arthritis. gamma delta T cells are significant producers of IL-17, thus the aim of this study was to investigate if E2 influenced IL-17(+) gamma delta T cells during arthritis development using a variety of experimental RA models: collagen-induced arthritis (CIA); antigen-induced arthritis (AIA); and collagen antibody-induced arthritis (CAIA). We demonstrate that E2 treatment decreases IL-17(+) gamma delta T cell number in joints, but increases IL-17(+) gamma delta T cells in draining lymph nodes, suggesting an E2-mediated prevention of IL-17(+) gamma delta T cell migration from lymph nodes to joints, in concert with our recently reported effects of E2 on Th17 cells (Andersson et al., 2015). E2 did neither influence the general gamma delta T cell population nor IFN gamma(+) gamma delta T cells, implying a selective regulation of IL-17-producing cells. In conclusion, this study contributes to the understanding of estrogen's role in autoimmune disease. (C) 2015 Elsevier Inc. All rights reserved.