人们对控制免疫球蛋白重链的同种异型决定簇的多态现象(polymorphisms)及其与某些自身免疫病发病基础的可能关系有浓厚兴趣。无疑,虽然大部分遗传易感性疾病,诸如Ⅰ型(胰岛素依赖型)糖尿病、自身免疫性甲状腺病和 Addison 病受 HLA 复合物中的基因决定,但这些疾病的免疫遗传基础仍有一些问题尚未解决。例如在Ⅰ型糖尿病先证者未受累的同胞兄弟姊妹中器官特异性抗体——经典的胰岛细胞抗体,甲状腺微粒体抗体和胃壁细胞抗体——的分布不受 HLA 遗传易感性的支配,而先证者则受 HLA 单型的支配。换言之,如果自身抗体的生成受遗传基因控制,显然它与有遗传倾向的胰腺 B 细胞损害并不相同。通过许多人群中免疫球蛋白同种异型的研究,发 There is a great deal of interest in polymorphisms controlling allosteric determinants of immunoglobulin heavy chains and their possible relationship to the underlying pathogenesis of certain autoimmune diseases. Undoubtedly, although most of the genetic predisposition to diseases, such as type I (insulin-dependent) diabetes, autoimmune thyroid disease and Addison’s disease, are determined by the genes in the HLA complex, some of the immunological genetic basis for these diseases remain unresolved . For example, the distribution of organ-specific antibodies - classical islet cell antibodies, thyroid microsomal antibodies and parietal cell antibodies - in sibling siblings not affected by type I diabetes probands is not dominated by genetic predisposition to HLA, Subjects are dominated by HLA haplotype. In other words, if the generation of autoantibodies is genetically controlled, it is clear that it is not the same as the genetic predisposition to pancreatic B-cell damage. Through the study of immunoglobulin allotypes in many populations,