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Receptors in Anti-Type II Collagen Antibody-Induced Arthritis
Biological Research Laboratories, Sankyo Co., Ltd., Shinagawa-ku, Tokyo, Japan
Anti-type II collagen (anti-CII) Ab is a well-known autoantibody observed in patients with rheumatoid arthritis. Injection of anti-CII Ab and LPS induces arthritis in mice in which anti-CII Ab as well as inflammatory cytokines, IL-1
and TNF-
, play critical roles. We investigated the involvement of IgG FcRs (Fc
Rs) in this arthritis model. BALB/c mice injected with the F(ab')2 of anti-CII Ab showed no signs of arthritis. Arthritis development was not observed in FcR-/- mice and was partially suppressed in FcRIII-/- mice despite the binding of anti-CII Ab and C3 to cartilage surface. Surprisingly, BALB/c mice lacking FcRIIB, which is known as an inhibitory FcR, developed arthritis with no exacerbation in arthritis score compared with wild-type (WT) mice, and only slight exacerbation was observed in the histopathological analysis. In contrast, aged FcRIIB-/- BALB/c mice developed arthritis without LPS injection, suggesting an augmented susceptibility to arthritis in aged FcRIIB-/- mice. No significant difference was observed among BALB/c-WT, -FcR-/-, and -FcRIIB-/- mice on cytokine production induced by anti-CII Ab and LPS injection. Severe arthritis developed in BALB/c-WT and -FcRIIB-/- mice, but not in BALB/c-FcR-/- mice, after the injection of anti-CII Ab and inflammatory cytokines. These results suggest that the reason behind the nondevelopment of arthritis in FcR-/- BALB/c mice is not due to a disorder in transient cytokine production, but to an irregularity downstream of cytokine production.
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