Interleukin 17-expressing Innate Synovial Cells Drive K/Bxn Serum-induced Arthritis.
- Author:
Wang Shik CHO
1
;
Eunkyeong JANG
;
Ho Youn KIM
;
Jeehee YOUN
Author Information
- Publication Type:Brief Communication
- Keywords: IL-17; Synovial cells; Arthritis; Immune complex
- MeSH: Animals; Antigen-Antibody Complex; Arthritis*; Autoantibodies; Interleukin-17; Interleukin-23; Interleukins*; Joints; Mice
- From:Immune Network 2016;16(6):366-372
- CountryRepublic of Korea
- Language:English
- Abstract: K/BxN serum can induce arthritis in normal mice because of abundant autoantibodies that trigger an innate inflammatory response in joints. To determine whether IL-17 is involved in the pathogenesis of serum-induced arthritis, we injected wild-type and IL-17(−/−) mice with K/BxN serum and evaluated them for signs of arthritis. Unlike wild-type mice, IL-17(−/−) mice did not show any signs of arthritis. IL-17 was produced predominantly by CD3⁻ CD4⁻γδTCR⁻ NK1.1⁻ Sca1(int) Thy1(hi) cells residing in the inflamed synovial tissue. When synovial cells extracted from normal joints were stimulated with IL-23 or autoantibody-containing immune complexes, a substantial fraction of Sca1(int) Thy1(hi) cells produced IL-17. Thus, we have identified a novel population of IL-17-producing innate synovial cells that play a crucial role in the development of K/BxN serum-induced arthritis.
