Willcox N, Demaine A G, Newsom-Davis J, Welsh K I, Robb S A, Spiro S G
Hum Immunol. 1985 Sep;14(1):29-36. doi: 10.1016/0198-8859(85)90062-x.
In view of the evidence for an autoimmune pathogenesis of the Lambert-Eaton myasthenic syndrome, we have sought associations with IgG heavy chain allotypes (Gm) and HLA antigens in 30 patients, of whom 20 had evidence of lung carcinoma (histologically proven small ("oat") cell type in 17). A highly significant overall increase in frequency of Glm(2) (chi 2 = 10.95; p less than 0.001; n = 30) and of HLA-B8 (chi 2 = 19.07; p less than 0.001; n = 23) was observed. These two factors apparently occurred independently of each other. The Glm(2) frequency in 36 non-myasthenic small cell carcinoma cases was the same as in a control panel (n = 167). We conclude that Glm(2) and HLA-B8 both associate with increased susceptibility to the Lambert-Eaton myasthenic syndrome, and suggest that Glm(2) may be in linkage disequilibrium with a limited number of VH genes coding for antibodies to restricted antigenic determinants at the nerve terminals, which may be shared by the carcinoma cells.
鉴于兰伯特 - 伊顿肌无力综合征存在自身免疫发病机制的证据，我们对30例患者进行了免疫球蛋白G重链同种异型（Gm）和人类白细胞抗原（HLA）抗原相关性研究，其中20例有肺癌证据（17例经组织学证实为小（“燕麦”）细胞型）。观察到G1m(2)频率总体显著增加（卡方 = 10.95；p < 0.001；n = 30）以及HLA - B8频率显著增加（卡方 = 19.07；p < 0.001；n = 23）。这两个因素显然相互独立出现。36例非肌无力性小细胞癌病例中的G1m(2)频率与一个对照组（n = 167）相同。我们得出结论，G1m(2)和HLA - B8均与兰伯特 - 伊顿肌无力综合征易感性增加相关，并提示G1m(2)可能与有限数量的可变区重链（VH）基因处于连锁不平衡状态，这些基因编码针对神经末梢受限抗原决定簇的抗体，而癌细胞可能共享这些抗原决定簇。
