Williams R C
Department of Medicine, University of Florida, Gainesville 32610.
Scand J Rheumatol Suppl. 1988;75:300-8. doi: 10.3109/03009748809096782.
Rheumatoid factors (RF) occur during the course of various infections such as leprosy, infective endocarditis, tuberculosis, trypanosomiasis, visceral larva migrans, infectious mononucleosis, influenza A, hepatitis A or cytomegalovirus. When first described it seemed logical to assume that host-self-immunization with autologous immune complexes provided the initial stimulus for RF production. Subsequently extensive characterization of bacterial, parasitic and viral Fc receptors has suggested an alternative explanation for rheumatoid factor associated with infections. It seems possible that patients make an initial immune response to infecting agent Fc receptors and that anti-anti-Fc receptors or anti-idiotypes either then directly stimulate rheumatoid factor production or are themselves rheumatoid factors. Such a hypothesis might also be applied to rheumatoid arthritis itself where either infecting agent or autologous cell Fc receptors could be the initial immunizing epitopes involved in rheumatoid factor production.
类风湿因子（RF）出现在各种感染过程中，如麻风病、感染性心内膜炎、结核病、锥虫病、内脏幼虫移行症、传染性单核细胞增多症、甲型流感、甲型肝炎或巨细胞病毒感染。最初描述时，认为自体免疫复合物引起的宿主自身免疫是RF产生的初始刺激似乎是合乎逻辑的。随后，对细菌、寄生虫和病毒Fc受体的广泛表征为与感染相关的类风湿因子提出了另一种解释。患者可能首先对感染因子Fc受体产生免疫反应，然后抗抗Fc受体或抗独特型抗体要么直接刺激类风湿因子的产生，要么自身就是类风湿因子。这样的假设也可能适用于类风湿关节炎本身，其中感染因子或自体细胞Fc受体可能是参与类风湿因子产生的初始免疫表位。
