Bonvoisin B
Sem Hop. 1984 May 3;60(19):1361-9.
Rheumatoid arthritis (RA) is an autoimmune disease whose diagnosis was long based solely upon the demonstration of rheumatoid factors (RF) which are IgM antibodies with anti-IgG specificity. The development of modern techniques which are more sensitive and/or detect non-IgM rheumatoid factors has reduced the percentage of presumptive seronegative RA. Immunological studies of the disease also reveal other evidences of polyclonal B-lymphocyte activation: hypergammaglobulinemia, high levels of beta-2-microglobulin and circulating immune complexes, presence of various autoantibodies (anti-collagen, antilymphocyte and, in some instances, anti-nuclear antibodies). These anomalies are found, not only in the blood, but above all in the synovial fluid, which explains the low synovial complement level. The disturbances of cellular immunity cannot yet be used for diagnostic purposes, but suggest that the physiopathologic mechanism of RA involves a decreased T-suppressor lymphocyte activity and/or B-cell unresponsiveness to suppressor influences.
类风湿性关节炎(RA)是一种自身免疫性疾病,其诊断长期以来仅基于类风湿因子(RF)的检测,类风湿因子是具有抗IgG特异性的IgM抗体。现代技术的发展更敏感和/或能检测非IgM类风湿因子,这降低了推定血清阴性RA的比例。对该疾病的免疫学研究还揭示了多克隆B淋巴细胞激活的其他证据:高球蛋白血症、高水平的β2微球蛋白和循环免疫复合物、各种自身抗体(抗胶原蛋白、抗淋巴细胞,在某些情况下还有抗核抗体)的存在。这些异常不仅在血液中发现,而且首先在滑液中发现,这解释了滑膜补体水平较低的原因。细胞免疫紊乱尚不能用于诊断目的,但提示RA的生理病理机制涉及T抑制淋巴细胞活性降低和/或B细胞对抑制性影响无反应。