The pathogenesis of Type 1 diabetes in children-the role of endogenous retrovirus infection in relation with disposition, environment and auto-immunity

在这两年中，我们研究了以下项目：1)从新诊断的酮症电话型1型糖尿病儿童中分离肠病毒mRNA：从新诊断的1型糖尿病儿童中提取95份血清和26份单核细胞样本，试图提取肠道病毒mRNA(VP4)，但没有一份血清样本和单核细胞样本未能分离病毒mRNA。2)在IDDMK_<1.2 bbb22的超抗原编码区，从初始甲硫酮编码码的290和461个核苷酸位置，我们发现了两个非同义的A/G多态性。Dr.Conrad B对超抗原活性和这种多态性感兴趣，并要求我们与1型糖尿病儿童合作。然而，由于种种原因，这些合作研究最终都没有成功。3)儿童慢进展型1型糖尿病（SPIDDM）的临床和遗传特征：我们分析了急性发作型1型糖尿病、SPIDDM、NIDDM和正常对照儿童的HLA DQ-β、-α基因、DR-β基因，以确定SPIDDM的发病机制。我们发现，SPIDDM的发病年龄比急性发病年龄大得多，胰岛抗体阳性几乎相同。HLA基因与NIDDM和对照组不同。DRB1 0405-DQB1 0401是流行的，将是1型糖尿病的一个亚型。

We have studied the following projects during these two years 1) Isolation of Enterovirus m RNA from newly diagnosis of ketosis-phone type 1 diabetic children : 95 serum and 26 mononuclear cells samples from newly diagnosis type 1 diabetes were tried to extract entero-virus mRNA(VP4), however non of the serum samples nor mononuclear cells were failed to isolate virus mRNA. 2) We identified two nonsynonymous A/G polymorphisms in the superantigen-coding region of IDDMK_<1.2>22 at the 290-and 461-nucleotide position from the initial methione coden. Dr.Conrad B was interested in relation to super -antigen activity and this polymorphism and asked us to collaborate with type 1 diabetic children. However, in some reason, these collaborate studies were finally not succeeded due to their reasons. 3) Clinical and genetic characteristic of slowly progressing type 1 diabetes(SPIDDM) in children : We have analyzed HLA DQ-β, -αgene, DR-βgene, in children with acute-onset type 1 diabetes, SPIDDM, NIDDM and normal controls to identified the pathogenesis of SPIDDM. We found that age at onset of SPIDDM is much elder than acute onset and positivity of islet antibodies was almost same. HLA genes were different from NIDDM and controls. DRB1 0405-DQB1 0401 is popular and will be a subtype of type 1 diabetes mellitus.