Trentham D E, Dynesius R A, Rocklin R E, David J R
Trans Assoc Am Physicians. 1978;91:118-28.
Using an assay to measure antigen-induction of a lymphocyte mediator, LIF, we detected cellular sensitivities to native human types II and III collagens in three-quarters of a group of 50 patients with rheumatoid arthritis. There was no cellular response to type I collagen. Cellular reactivities to collagen were absent in a group of 41 patients who had other kinds of arthritis, such as osteoarthritis, crystalline-induced synovitis, or arthropathies associated with a high prevalence of the HLA-B27 antigen. Lymphocytes, responding to an unknown persistent antigenic stimulus, are thought to play a major role in the pathogenesis of rheumatoid arthritis. It has previously been hypothesized that collagen might function as an autoantigen in this disease. Based on the disease specificity of our findings and the tissue distribution of types II and III collagens, we propose that cellular sensitivities to these structural proteins may be involved in the pathogenesis of rheumatoid arthritis.
我们运用一种检测淋巴细胞介质LIF抗原诱导作用的分析方法，在一组50例类风湿关节炎患者中，检测到四分之三的患者对天然人II型和III型胶原存在细胞敏感性。对I型胶原无细胞反应。在一组41例患有其他类型关节炎（如骨关节炎、晶体诱导性滑膜炎或与HLA - B27抗原高患病率相关的关节病）的患者中，未发现对胶原的细胞反应。人们认为，对未知持续抗原刺激作出反应的淋巴细胞在类风湿关节炎的发病机制中起主要作用。此前曾有人提出，胶原可能在这种疾病中作为自身抗原发挥作用。基于我们研究结果的疾病特异性以及II型和III型胶原的组织分布，我们提出对这些结构蛋白的细胞敏感性可能参与了类风湿关节炎的发病机制。
