Holmdahl R, Mo J, Nordling C, Larsson P, Jansson L, Goldschmidt T, Andersson M, Klareskog L
Department of Medical and Physiological Chemistry, Uppsala University, Sweden.
Clin Exp Rheumatol. 1989 Sep-Oct;7 Suppl 3:S51-5.
The type II collagen induced arthritis animal model (CIA) provides opportunities to study the nature of autoimmune reactions leading to arthritis and is also a useful model for rheumatoid arthritis (RA). Thus, in similarity with RA, the CIA when induced with autologous type II collagen, 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 autoantibodies to type II collagen and rheumatoid factors are produced. Immunohistopathology of affected joints show in both diseases a dominance of activated macrophages/fibroblasts with a significant infiltration of activated T cells. We suggest here that both RA and CIA are dependent on a synergy between delayed type hypersensitivity and immune complex mediated inflammatory mechanisms and that CIA could provide a tool for studies of immunospecific reactions leading to arthritis.
II型胶原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，也是类风湿性关节炎（RA）的有用模型。因此，与RA相似，用自体II型胶原诱导的CIA表现出慢性和进行性的病程。对RA和CIA的易感性都与某些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II型胶原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/成纤维细胞占主导地位，并有大量活化T细胞浸润。我们在此提出，RA和CIA都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可以为研究导致关节炎的免疫特异性反应提供一个工具。
