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IL-17-producing γδT cells are regulated by estrogen during development of experimental arthritis.

Journal article
Authors Annica Andersson
Louise Grahnemo
Cecilia Engdahl
Alexandra Stubelius
Marie K Lagerquist
Hans Carlsten
Ulrika Islander
Published in Clinical immunology (Orlando, Fla.)
Volume 161
Issue 2
Pages 324-32
ISSN 1521-7035
Publication year 2015
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Centre for Bone and Arthritis Research
Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Pages 324-32
Language en
Links dx.doi.org/10.1016/j.clim.2015.09.0...
Subject categories Rheumatology and Autoimmunity

Abstract

Interleukin-17 (IL-17) drives inflammation and destruction of joints in rheumatoid arthritis (RA). The female sex hormone 17β-estradiol (E2) inhibits experimental arthritis. γδT cells are significant producers of IL-17, thus the aim of this study was to investigate if E2 influenced IL-17(+) γδT 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(+) γδT cell number in joints, but increases IL-17(+) γδT cells in draining lymph nodes, suggesting an E2-mediated prevention of IL-17(+) γδT 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 γδT cell population nor IFNγ(+) γδT 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.

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