The role of IL-4 in regulation of murine collagen-induced arthritis
The role of IL-4 in regulation of murine collagen-induced arthritis
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DOI：
10.1006/clim.2001.5162
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发表时间：
2002-02-01
影响因子：
8.6
通讯作者：
Kang, AH
中科院分区：
文献类型：
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作者：
Myers, LK;Tang, B;Kang, AH
胶原诱导的关节炎（CIA）是一种自身免疫介导的多关节炎的小鼠模型。可以通过（静脉注射）CH 诱导产生 Th2 细胞因子的调节性 CD4(+) T 细胞来预防 CIA。然而，IL-4 在抑制关节炎方面的相对重要性仍不清楚。为了解决这个问题，对用耐受的 CH 特异性细胞治疗的小鼠给予 IL-4 的中和单克隆抗体。该抗体显着逆转了预期的关节炎抑制作用。此外，对DBA/1 IL4(-/-)小鼠（通过将C57B1/6 IL4(-/-)与野生型DBA/1小鼠回交而产生）静脉内施用CH在抑制疾病方面完全无效。这些数据支持 IL-4 在调节自身免疫性关节炎中的重要性。观察到其他 Th2 细胞因子的 mRNA 信息代偿性增加，但它们并没有恢复对关节炎的抑制。 IL4(-/-) 小鼠的 CH 抗体（主要是 IgG2a）增加。这些研究提供了一个独特的机会来分析 IL-4 的作用及其在自身免疫小鼠关节炎模型中的缺失。 (C) 2002 年爱思唯尔科学（美国）。
Collagen-induced arthritis (CIA) is a murine model of autoimmune-mediated polyarthritis. CIA can be prevented by the administration (intravenously) of CH, inducing regulatory CD4(+) T cells which produce Th2 cytokines. However, the relative importance of IL-4 in suppressing arthritis remains unclear. To address this question, a neutralizing monoclonal antibody to IL-4 was given to mice treated with tolerized, CH-specific cells. The antibody significantly reversed the expected suppression of arthritis. Moreover, CH administered intravenously to DBA/1 IL4(-/-) mice (developed by backcrossing C57B1/6 IL4(-/-) to wild-type DBA/1 mice) was completely ineffective in suppressing disease. These data support the importance of IL-4 in the regulation of autoimmune arthritis. Compensatory increases in mRNA message for other Th2 cytokines were observed, but they did not restore suppression of arthritis. Antibodies to CH, mostly IgG2a, were increased in IL4(-/-) mice. These studies represent a unique opportunity to analyze the role of IL-4 and its absence on an autoimmune murine model of arthritis. (C) 2002 Elsevier Science (USA).