Collagen-induced arthritis (CIA) in mice is animal model of autoimmune disease known as rheumatic arthritis in human. We investigated CII-specific CD4+ T cell receptor usage in CIA mice.

In CIA model, draining lymph node (dLN) CD4+ T cells and splenocytes at 3^rd, 5^th, 8^th week, we investigated CII-specific T cell proliferation, production of IL-17, IFN-γ, TNF-α, IL-4 and IL-10. And we also performed anti-CII IgG Ab measurements in serum level, TCRVβ usage and T cell clonality with RT-PCR-SSCP analysis. Also, we performed proliferative response against CII when CII-specific T cell subset is deleted.

CIA mice showed more increase in the serum level of anti-CII IgG than normal mice after induction of arthritis. And the level of anti-CII IgG2a in CIA mice was increased after 3^rd week after primary immunization, while anti-CII IgG1 was decreased. Draining LN CD4+T cells have proliferated against CII stimulation at 3^rd week after 1^st immunization. CD4+T cells derived from dLN of CIA mice produced proinflammatory cytokine IFN-γ, IL-17 etc. Draining LN CD4 T cells of CIA presented higher proportion of CD4+Vβ3+subsets compared to those of normal mice at 3^rd week after 1^st immunization, and they were increased in proportion by CII stimulation. Draining LN CD4+ T cells without TCRV β3+/Vβ8.1/8.2+/Vβ10b+cells were not responsive against CII stimulation. But, CII-reactive response of TCRVβ3-/Vβ8.1/8.2-/Vβ10b- T cells was recovered when Vβ3+ T cells were added in culture.

Our results indicate that CD4 +Vβ3+ T cells cells are selectively expanded in dLN of CIA mice, and their recovery upon CII re-stimulation in vitro, as well as the production Th1-type cytokines, may play pivotal role in CIA pathogenesis.