Diabetes Perdiction in Skane(DiPiS)

1型糖尿病（T1 DM）发生于遗传易感个体。有很强 疾病与环境因素有关，这些因素被认为是引发疾病的原因。的 疾病的发病机制依赖于自身免疫现象， 体液免疫应答直接针对β细胞中的几种自身抗原。这种疾病有一个 长前驱症状和GAD 65、IA-2或胰岛素自身抗体的出现预示疾病。在 目前的研究-糖尿病预测在Skane（DiPiS），我们将筛选所有新生儿（约10，000 高危HLA和其他TIDM遗传因素。胰岛细胞自身抗体 将在出生时和随访期间分析IA-2和胰岛素对GAD 65的影响， 环境触发器特别是，我们将检验妊娠不良事件 代表胰岛自身免疫的触发因素，将进展为1型糖尿病，但仅在一些 易受感染的对象具体目标是：1）对南部SkSne的所有新生儿进行筛查， 瑞典的一个地区，有120万居民; 2）分析脐带血中的1型糖尿病 高危HLA等位基因和三种胰岛细胞自身抗体GAD 65 Ab、IAA和IA-2 Ab; 3） 分析感染史、妊娠不良事件和心理社会因素作为附加因素，或 妊娠期1型糖尿病风险的增强因素沿着病毒PCR和血清学; 4)确定GAD 65、IA-2和胰岛素自身抗体的同种型、亚型和表位特异性 出生时，首次出现自身抗体时和1型糖尿病诊断时; 5） 确定健康母亲所生新生儿的自身抗原反应性T细胞， 自身抗体作为自身免疫暴露的证据，以及6）向数据库提交关键数据 协调中心（DCC），以有效地识别环境触发1型糖尿病。的i 长期目标是确定妊娠期感染或其他不良事件的作用， 心理因素增加了遗传易感儿童患1型糖尿病的风险。 了解遗传风险和环境风险因素之间的相互作用， 制定减少接触的战略，从而最大限度地减少糖尿病风险。

Type 1 diabetes mellitus (T1DM) develops in genetically susceptible individuals. There is a strong disease association with environmental factors, which are thought to trigger the disease. The disease pathogenesis is dependent on autoimmune phenomena involving both the cellular and humoral immune response direct against several autoantigens in the beta cells. The disease has a long prodrome and the appearance of GAD65, IA-2 or insulin autoantibodies predict disease. In the present study - Diabetes Prediction in Skane (DiPiS) we will screen all newborns (about 10, 000 children per year) for high risk HLA and other TIDM genetic factors. Islet cell autoantibodies against GAD65, IA-2 and insulin will be analyzed at birth and during follow-up to identify environmental triggers. In particular, we will test the hypothesis that gestational adverse events represents triggers of islet autoimmunity that will progress to type 1 diabetes but only in some susceptible subjects. The Specific aims are: 1) to screen all newborn babies in SkSne, the Southern region of Sweden with 1.2 million inhabitants; 2) to analyze the cord blood for type 1 diabetes high risk HLA alleles and for the three islet cell autoantibodies, GAD65Ab, IAA and IA-2Ab; 3) to analyze infectious history, gestational adverse events and psychosocial factors as additive or potentiating factors to type 1 diabetes risk along with virus PCR and serology during pregnancy; 4) to define isotype, subtype and epitope specificities of autoantibodies to GAD65, IA-2 and insulin at birth, at the first appearance of autoantibodies and at diagnosis of type 1 diabetes; 5) to determine autoantigen reactive T cells in neonates born to healthy mothers positive for autoantibodies as evidence of autoimmunity exposure and 6) to submit critical data to the Data Coordinating Center (DCC) to effectively identify environmental triggers of type 1 diabetes. The i long-term objective is to identify the role of gestational infections or other adverse events and i psychological factors that increase the risk for type 1 diabetes in genetically susceptible children. Understanding the interaction between genetic risk and environmental risk factors may permit the development of strategies to reduced exposure and thereby minimize diabetes risk.