论文部分内容阅读
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 induce multiple arthritis of DBA / 1 mice immunized with type Ⅱcollagen (CⅡ) and to observe the effects of interleukin-1 (IL-1) on IL-1 The impact of arthritis. Methods The mice were injected intracranially with complete Freund’s adjuvant (CFA). The mice were injected intradermally with IL-1 at day 18 after CII immunization. Happening. Serum anti-CⅡ antibody was detected by ELISA, and histopathological analysis of the occurrence and severity of the disease was performed. Results All of the mice inoculated with CⅡ and CFA developed multiple arthritis, but none of the control mice inoculated with CFA alone. Incidence of mouse serum anti-C Ⅱ high level of anti-antibody production. Histological analysis showed that pathological changes in the lesions of mice treated with IL-1 were more severe than those in the untreated mice. Conclusion C Ⅱ induced collagen induced arthritis (CIA) in DBA / 1 mice. IL-1 can promote arthritis in the formation of various inflammatory events.