摘要
目的 探讨类风湿性关节炎 (RA)发病的免疫学机制以及II型胶原在疾病发生过程中的作用。方法 用鸡Ⅱ型胶原 (CCⅡ )加完全佛氏佐剂 (CFA)免疫Wistar大鼠建立胶原诱导性关节炎 (CIA)模型 ,分别用发病大鼠的T淋巴细胞和血清进行过继转移 ;以ELISA检测外周血中抗CCⅡ抗体的水平 ;用病理组织学方法对炎性关节进行分析。结果 成功建立了CIA大鼠模型 ,发病率为 90 %。用T淋巴细胞转移的大鼠 ,可见明显CIA症状 ,发病率为 4 0 % ;实验组大鼠外周血中的抗CCⅡ抗体的水平虽较对照组高 ,但并无显著性意义 (P >0 .0 5 )。以血清过继转移的大鼠无一发病 ,但该组外周血中抗CCⅡ抗体的水平明显高于对照组 (P <0 .0 5 ) ;组织学鉴定结果可见炎性部位呈典型的CIA病变。结论 CIA可以通过淋巴细胞过继转移 ,机体对Ⅱ型胶原产生的特异性细胞免疫应答在CIA发生过程中起着重要的作用 。
Objective To investigate the immunological mechanism and the role of the type Ⅱ collagen in the causation of rheumatoid arthritis(RA). Methods To establish the animal model with type Ⅱ collagen induced arthritis(CIA). Wistar rats were immunized by intra dermal injection of chicken collagen Ⅱ(CCⅡ) in Freund's complete adjuvant(CFA). The T lymphocytes and serum of rats with CIA were adop tively transferred, respectively. The level of anti CCⅡ antibody and the degree of disease were analyzed by ELISA and pathological histology, respectively. Results The CIA model was established successfully. The clinical expression can be seen in the rats transferred with T cells and the incidence was 40%. The level of anti CCⅡ antibody was slight higher than that of control, but the differentiation has no significance ( P >0.05). All of the rats transferred with serum showed no appearance of CIA, but the level of anti CCⅡ antibody was significantly higher than that of control ( P <0.05). The analysis of the pathological histology showed the typical arthritis. Conclusions CIA can be induced by adoptive transfer with lymphocytes and the type Ⅱ collagen(CⅡ) specific cellular immunological response play an essential role in the causation of RA and provide the basis for treatment of RA with immunologic method mediated by T cells. [
出处
《免疫学杂志》
CAS
CSCD
北大核心
2002年第1期9-12,共4页
Immunological Journal
基金
国家自然科学基金资助项目 (39770 70 5 )
