Dellagi K, Brouet J C, Danon F
J Clin Invest. 1979 Nov;64(5):1530-4. doi: 10.1172/JCI109612.
The monoclonal immunoglobulin (Ig)M from 5 to 16 patients with Waldenström's macroglobulinemia and a polyneuropathy shared cross-idiotypic antigenic determinants as demonstrated by hemagglutination and hemagglutination inhibition experiments as well as by precipitin reactions. This reactivity was located to the Fab (and not Fc) fragment of the protein. The IgM from 73 patients with macroglobulinemia but without neuropathy all gave negative reactions. In contrast, the monoclonal IgG from a patient with polyneuropathy also possessed similar idiotypic determinants. Since cross-idiotypic determinants are usually related to the combining site of a monoclonal Ig, this finding suggests that the monoclonal Ig of these patients may mediate the nerve injury via their antibody activity, which could be directed either to a nerve antigen or to some component involved in the pathogenesis of the neuropathy.
通过血凝、血凝抑制实验以及沉淀反应证明,5至16例华氏巨球蛋白血症伴多发性神经病患者的单克隆免疫球蛋白(Ig)M具有共同的交叉独特型抗原决定簇。这种反应性定位于该蛋白的Fab(而非Fc)片段。73例无神经病的巨球蛋白血症患者的IgM均呈阴性反应。相比之下,1例多发性神经病患者的单克隆IgG也具有相似的独特型决定簇。由于交叉独特型决定簇通常与单克隆Ig的结合位点相关,这一发现表明这些患者的单克隆Ig可能通过其抗体活性介导神经损伤,该抗体活性可能针对神经抗原或参与神经病发病机制的某些成分。