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目的 以Ⅱ型胶原(TYPE ⅡCOLLAGEN,CⅡ) 免疫接种DBA/1 小鼠,诱发其多发性关节炎发生,并以白细胞介素1(INTERLEUKIN -1,IL- 1)皮内注射,观察IL- 1 对关节炎发生的影响.方法 采用CⅡ加弗氏完全佐剂(COMPLETEFREUND○S ADJUVANT,CFA) 给小鼠行皮内注射,并于CⅡ免疫接种后第18 天开始,给部分小鼠皮内注射IL- 1,观察其发病情况.采用ELISA 方法检测血清抗CⅡ抗体,并对疾病的发生及严重程度进行组织病理学分析.结果 所有接种CⅡ和CFA 的小鼠均发生了多发性关节炎,而只接种CFA 的对照组小鼠无一发病.发病小鼠血清中有高水平的抗CⅡ抗体产生.组织学分析结果显示,经IL-1 处理的小鼠病变部位病理学改变较未处理者更为严重.结论 CⅡ可诱发DBA/1 小鼠产生胶原诱导的关节炎(COLLAGENINDUCED ARTHRITIS,CIA) .IL- 1 有促进关节炎形成过程中的各种炎性事件发生的作用.“,”Objective To observe the effect of interleukin-1 (IL-1) on collagen induced arthritis. Methods The multiple arthritis in DBA/1 mice was induced by immunized with native typeⅡcollagen(CⅡ) ;IL-1 was injected intradermally to observe its effect on collagen induced arthritis (CIA) 18 days later. Serum antibody to CⅡwas measured by ELISA. Disease incidence and severity were assessed by clinical index and histological features. Results All of the mice immunized with CⅡdeveloped CIA, but no one immunized with complete freunds adjuvant(CFA) had CIA. The levels of anti CⅡantibody in serum of CIA mice were higher than that in the control. Incidence and severity of CIA in mice treated with IL-1 are more significant than those without treatment. Conclusion CⅡcan induce CIA in DBA/1 mice. The development of CIA in DBA/1 mice was accelerated by IL-1.