Mutation at H–2K locus influences susceptibility to autoimmune thyroiditis
Mutation at H–2K locus influences susceptibility to autoimmune thyroiditis
复制标题
H–2K 位点突变影响自身免疫性甲状腺炎的易感性
作者：
R. Maron;I. Cohen
已发现主要组织相容性复合体（MHC）中的基因与自身免疫性疾病的发生相关，包括人类的自发性疾病1，2和动物的自发性疾病3或实验诱导的自身免疫性疾病4。实验性自身免疫性甲状腺炎（EAT）可以在易感品系的小鼠中诱导，例如具有MHC H-2k单倍型的小鼠，通过将小鼠甲状腺球蛋白与完全弗氏佐剂一起注射5。相反，注射H-2b单倍型纯合子小鼠不能诱导EAT特征性甲状腺单核细胞浸润。我们在这里报告的易感性诱导EAT的结果从一个明显的点突变，显然发生在H-2K位点的抗性H-2b单倍型。这表明H-2K糖蛋白可以调节对甲状腺球蛋白的自身免疫反应。
GENES in the major histocompatibility complex (MHC) have been found to be associated with the development of autoimmune diseases, including spontaneous diseases in man1,2 and spontaneous3 or experimentally induced autoimmunity in animals4. Experimental autoimmune thyroiditis (EAT) can be induced in susceptible strains of mice, such as those with the MHC H–2k haplotype, by injecting them with mouse thyroglobulin together with complete Freund's adjuvant5. In contrast, injection of mice homozygous for the H–2b haplotype fails to induce the mononuclear cell infiltration of the thyroid gland characteristic of EAT. We report here that susceptibility to induction of EAT results from an apparent point mutation which evidently occurred at the H–2K locus of the resistant H–2b haplotype. This indicates that the H–2K glycoprotein can serve to regulate the autoimmune response to thyroglobulin.