Holmdahl R, Andersson M E, Goldschmidt T J, Jansson L, Karlsson M, Malmström V, Mo J
Department of Medical and Physiological Chemistry, Uppsala University, Sweden.
APMIS. 1989 Jul;97(7):575-84. doi: 10.1111/j.1699-0463.1989.tb00446.x.
The type II collagen (CII) induced arthritis animal model (CIA) provides opportunities to study the nature of autoimmune reactions leading to arthritis and may be used as a model for rheumatoid arthritis (RA). Thus, in similarity with RA, the CIA model, when induced with autologous CII, shows a chronic and progressive disease course. The susceptibility to both RA and CIA are correlated to the expression of certain MHC class II allotype genes. In both diseases are autoantibodies to CII and rheumatoid factors produced. Immunohistopathology of affected joints show in both diseases a dominance of activated macrophages/fibroblasts with a significant infiltration of activated T cells and an infiltration of granulocytes. We do here suggest that both RA and CIA are dependent on a synergy between delayed type hypersensitivity and immune complex mediated inflammatory mechanisms and that CIA provides opportunities for studies of immunospecific reactions leading to arthritis.
II型胶原（CII）诱导的关节炎动物模型（CIA）为研究导致关节炎的自身免疫反应的本质提供了机会，并且可作为类风湿性关节炎（RA）的模型。因此，与RA相似，当用自体CII诱导时，CIA模型呈现慢性和进行性病程。对RA和CIA的易感性均与某些MHC II类同种异型基因的表达相关。在这两种疾病中都会产生针对CII的自身抗体和类风湿因子。受累关节的免疫组织病理学显示，在这两种疾病中，活化的巨噬细胞/成纤维细胞占主导，伴有活化T细胞的显著浸润和粒细胞浸润。我们在此提出，RA和CIA均依赖于迟发型超敏反应和免疫复合物介导的炎症机制之间的协同作用，并且CIA为研究导致关节炎的免疫特异性反应提供了机会。
