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巨噬细胞移动抑制因子参与小鼠Ⅱ型胶原诱导性关节炎的发病机制。

Macrophage migration inhibitory factor is involved in the pathogenesis of collagen type II-induced arthritis in mice.

作者信息

Mikulowska A, Metz C N, Bucala R, Holmdahl R

机构信息

Department of Cell and Molecular Biology, Lund University, Sweden.

出版信息

J Immunol. 1997 Jun 1;158(11):5514-7.

PMID:9164975
Abstract

To determine the importance of macrophage migration inhibitory factor (MIF) in the development of arthritis we used an experimental model for rheumatoid arthritis, collagen type II (CII)-induced arthritis in mice. Treatment with neutralizing anti-MIF Abs before immunization of (B10.Q x DBA/1)F1 with CII led to delayed onset and lowered frequency of arthritis. This was associated with lower levels of IgG2a to CII in MIF-depleted mice. The proliferative response to CII was stronger in the anti-MIF-treated mice, whereas no significant effects were seen on Ag-induced IFN-gamma production in response to CII or on the total serum Ab levels in response to CII. These results provide the first experimental evidence of a role for MIF in the pathogenesis of autoimmune disease.

摘要

为了确定巨噬细胞移动抑制因子(MIF)在关节炎发展过程中的重要性,我们使用了类风湿性关节炎的实验模型,即小鼠Ⅱ型胶原(CII)诱导的关节炎。在用CII免疫(B10.Q×DBA/1)F1小鼠之前,用中和性抗MIF抗体进行治疗,可导致关节炎的发病延迟且发病率降低。这与MIF缺失小鼠中针对CII的IgG2a水平较低有关。抗MIF治疗的小鼠对CII的增殖反应更强,而对于CII刺激的Ag诱导的IFN-γ产生或对CII刺激的总血清抗体水平均未观察到显著影响。这些结果首次提供了实验证据,证明MIF在自身免疫性疾病的发病机制中发挥作用。

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