Abstract
In the present study, we examined the effect of interleukin 12 (IL-12) on the evolution of murine type II collagen-induced arthritis (CIA) . CIA mice injected intraperitoneally with IL-12 (500ng / mouse /d) demonstrated delayed onset and reduced severity of arthritis. Although IL-12 administration augmented lymphocyte proliferation and interferon-γ production against specific and non-specific stimulation, anti-collagen antibody production was significantly suppressed in CIA, as compared with control mice. Since IL-12 induced the production of serum tumor necrosis factor (TNF) -α and corticosterone, the suppression of CIA by IL-12 may, in part, depend upon the augmentation of serum corticosterone, induced by endogenous TNF-α.
These data suggest that IL-12 is an important immunomodulator of the pathogenesis of CIA, which acts by regulating not only the humoral and cellular immune responses, but also the expression of immunoregulatory mediators.
