Koopman W J, Gay S
Department of Medicine, University of Alabama School of Medicine, University of Alabama at Birmingham 35294.
Scand J Rheumatol Suppl. 1988;75:284-9. doi: 10.3109/03009748809096780.
Autoimmune MRL-lpr/lpr mice develop a spontaneous destructive arthropathy sharing some features with rheumatoid arthritis including synovial cell proliferation, pannus formation, rheumatoid nodule-like lesions and circulating rheumatoid factors. Rheumatoid factors elaborated by MRL-lpr/lpr mice exhibit binding characteristics similar to those found in the sera of patients with rheumatoid arthritis; however, these autoantibodies do not appear to be essential for the induction of arthritis in MRL-lpr/lpr mice. Molecular studies, indicating that VH genes from several VH families are capable of encoding these rheumatoid factors, argue against the existence of unique "autoantibody genes" in the germline of MRL-lpr/lpr mice. Although the mechanisms underlying cartilage injury in MRL-lpr/lpr mice have not been elucidated, available evidence suggests that invading synovial cells play an important role. Delineation of the cellular and molecular mechanisms responsible for articular destruction in MRL-lpr/lpr mice may provide important insights concerning the pathogenesis of rheumatoid arthritis.
自身免疫性MRL-lpr/lpr小鼠会自发发展出一种破坏性关节病，与类风湿性关节炎有一些共同特征，包括滑膜细胞增殖、血管翳形成、类风湿结节样病变以及循环类风湿因子。MRL-lpr/lpr小鼠产生的类风湿因子表现出与类风湿性关节炎患者血清中发现的类风湿因子相似的结合特性；然而，这些自身抗体似乎并非MRL-lpr/lpr小鼠关节炎诱导所必需。分子研究表明，来自几个VH家族的VH基因能够编码这些类风湿因子，这与MRL-lpr/lpr小鼠种系中存在独特“自身抗体基因”的观点相悖。尽管MRL-lpr/lpr小鼠软骨损伤的潜在机制尚未阐明，但现有证据表明，侵入的滑膜细胞起重要作用。阐明MRL-lpr/lpr小鼠关节破坏的细胞和分子机制可能为类风湿性关节炎的发病机制提供重要见解。
