I型糖尿病患者具有特异性组织相容抗原(HLA)及抗胰岛抗体,且胰岛内有淋巴细胞浸润等自身免疫性疾病的特征。Eisenbarth提出该病免疫改变的6个过程: 1期(遗传因素):95%患者特异性HLA阳性,常人仅5%。免疫球蛋白Ⅱ(classⅡ)抗原HLA—DQβ键57号位天冬氨酸为其他氨基酸代替。2期(环境因素):有许多与β细胞亲合力很强的病毒与化学物质。患者体内可发现效价很高的柯萨奇B_4IgM中和抗体。20%患者有先天性风疹史。仅用少量链脲菌素即可引起胰岛炎(insulitis),诱发自身免疫性β细胞损害。环境因素诱发自身免疫反应的机制尚不明,但β细胞表面发现MHC(主要组织相容复 Patients with type I diabetes mellitus have specific histocompatibility antigens (HLA) and anti-islet antibodies, and islet features such as lymphocyte infiltration and other autoimmune diseases. Eisenbarth proposed six changes in the immune response to the disease: stage 1 (genetic): 95% patient-specific HLA-positive, only 5% of normal people. Immunoglobulin Ⅱ (class Ⅱ) antigen HLA-DQβ bond number 57 aspartic acid instead of other amino acids. Phase 2 (environmental factors): There are many viruses and chemicals that have strong affinity for beta cells. In patients with high potency Coxsackie B_4IgM neutralizing antibodies can be found. 20% of patients have a history of congenital rubella. Only a small amount of streptozotocin can cause insulitis, inducing autoimmune beta-cell damage. The mechanism by which environmental factors induce the autoimmune response is not known, but MHC (major histocompatibility complex