Suppression of Immune Induction of Collagen-Induced Arthritis in IL-17-Deficient Mice

TLDR

Interleukin‑17, a T‑cell–derived proinflammatory cytokine, is implicated in rheumatoid arthritis but its pathogenic role remains unclear. The study evaluated collagen‑induced arthritis in IL‑17‑deficient (IL‑17−/−) mice to assess the cytokine’s contribution. IL‑17 deficiency markedly suppressed CIA, indicating IL‑17 drives collagen‑specific T‑cell priming and IgG2a production, thereby promoting disease.

Abstract

Abstract Interleukin-17 is a T cell-derived proinflammatory cytokine. This cytokine is suspected to be involved in the development of rheumatoid arthritis (RA) because this cytokine expression is augmented in synovial tissues of RA patients. The pathogenic roles of IL-17 in the development of RA, however, still remain to be elucidated. In this study, effects of IL-17 deficiency on collagen-induced arthritis (CIA) model were examined using IL-17-deficient mice (IL-17−/− mice). We found that CIA was markedly suppressed in IL-17−/− mice. IL-17 was responsible for the priming of collagen-specific T cells and collagen-specific IgG2a production. Thus, these observations suggest that IL-17 plays a crucial role in the development of CIA by activating autoantigen-specific cellular and humoral immune responses.