Rheumatoid factor cross idiotypes.
Rheumatoid factor cross idiotypes.
复制标题
类风湿因子交叉独特型。
DOI：
10.1007/bf01857225
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发表时间：
1988
期刊：
影响因子：
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通讯作者：
Agnello,V
中科院分区：
文献类型：
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作者：
Agnello,V
类风湿因子(RFS)在类风湿关节炎患者的血清中被发现已有50年的历史，但我们仍然不知道这些抗体的来源，也不确定它们在类风湿关节炎和其他疾病中的作用。考虑到关于RFs起源的理论的演变，奇怪的是，这些抗体最初被认为是由链球菌感染诱导的[15]。随着证据的积累显示RFS与聚集的免疫球蛋白的反应性，形成了RFS是复杂或改变的免疫球蛋白的抗体的概念。20世纪60年代初，S对亨利·昆克尔的研究表明，RFs与正常的单体免疫球蛋白反应，高浓度的单体免疫球蛋白抑制聚集的免疫球蛋白与RF的反应，推翻了这一假说[22，27，38，39]。除极少数例外，RFS与天然单体免疫球蛋白反应。与聚集的免疫球蛋白反应更强的原因是，与单体免疫球蛋白的单一结合部位相比，与复杂免疫球蛋白上的多个抗原结合部位反应时，免疫球蛋白RF的5个结合部位对亲和力的倍增效应。多年来流行的概念是，RFs是发生在类风湿性关节炎和其他自身免疫性疾病中的免疫球蛋白抗体。一项质疑这一概念的观察是在亚急性细菌性心内膜炎中检测到RFs[41]。这一观察刺激了查尔斯·克里斯蒂安在20世纪60年代末对S的研究，在他的研究中，他用大肠杆菌对兔子进行了高度免疫，并产生了RF[18]。这导致了一种概念，即RFs是由循环免疫复合体诱导的，并提出了RFs可能不仅是在病理状态下产生的抗体，也可能是在生理过程中产生的抗体，如循环免疫复合物的免疫清除。在研究兔对链球菌细胞壁抗原的免疫反应的遗传学时，Victor Bokisch做了一个很少受到关注的观察[10]。他发现一只兔子产生了7S RF，与链球菌细胞壁抗原发生交叉反应。这一观察结果回顾了细菌抗原诱导RF的原始理论，并再次支持了RF可能是由不同于免疫球蛋白的抗原产生的推测。再来一次
It has been 50 years since rheumatoid factors (RFs) were discovered in the sera of patients with rheumatoid arthritis, but we still do not know the origin of these antibodies that react with IgG, nor do we know with certainty their role in rheumatoid arthritis and other diseases in which they occur. Considering the evolution of theories on the origin of RFs, it is curious that these antibodies were originally thought to be induced by streptococcal infection [15]. With the accumulation of evidence showing the reactivity of RFs with aggregated IgG, the concept evolved that RFs were antibodies to complexed or altered IgG. The studies of Henry Kunkel in the early 1960's, which showed that RFs reacted with normal monomeric IgG and that in high concentration monomeric IgG could inhibit the reaction between aggregated IgG and RF, disproved this hypothesis [22, 27, 38, 39]. With rare exception, RFs react with native monomeric IgG. The greater reactivity with aggregated IgG results from the multiplier effect on affinity from the five combining sites of IgM RF when it reacts with multiple antigenic sites present on complex IgG compared with the single site on monomeric IgG. The prevailing concept for many years was that RFs were autoantibodies to IgG that occurred in rheumatoid arthritis and other autoimmune diseases. An observation that questioned this concept was the detection of RFs in sub acute bacterial endocarditis [41]. This observation stimulated the studies of Charles Christian in the late 1960's in which he hyperimmunized rabbits with E. coli bacteria and produced RFs [18]. This led to the concept that RFs were induced by circulating immune complexes and raised the possibility that RFs may be antibodies produced not only in pathological states but also during physiological processes, such as immune elimination of circulating immune complexes. An observation that received little attention was made by Victor Bokisch during studies on the genetics of the immune response to streptococcal cell wall antigens in rabbits [10]. He found a rabbit that produced a 7S RF that cross-reacted with streptococcal cell wall antigen. This observation recalled the original theory that bacterial antigens induced RFs and again promoted the speculation that RF may be produced by antigens other than those on IgG. Another more