SCREENING OF NEWBORNS/CHILDREN TO IDENTIFY SUBJECTS AT HIGH RISK FOR IDD

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 遗传、免疫和外源性因素相互作用，在少数具有发生胰岛素依赖型糖尿病（IDDM）遗传倾向的个体中诱导胰腺β细胞自身免疫。 我们过去的研究证明，临床前IDDM可以在儿童和成人中通过免疫和代谢标志物来识别。 他们还证明，在高风险个体中持续产生针对β细胞抗原的自身抗体几乎总是在研究入组之前开始。 因此，我们假设自身免疫级联反应的启动以及由此产生的最终导致临床疾病的分子和细胞变化发生在生命的最初几年。 因为它在婴儿最早产生自身抗体之前识别出β细胞自身免疫的高风险婴儿，我们的新生儿遗传筛查计划为我们提供了有史以来第一次在队列设计中测试假设的机会。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Genetic, immunological, and exogenous factors interact to induce pancreatic beta-cells autoimmunity in a small minority of the individuals who have a genetic predisposition to developing insulin-dependent diabetes mellitus (IDDM). Our past studies proved that preclinical IDDM could be identified in children and adults with immune and metabolic markers. They also demonstrated that persistent production of autoantibodies against beta-cell antigens in high-risk individuals almost always commenced prior to the time of study enrollment. We therefore hypothesize that the initiation of the autoimmune cascade and the resultant molecular and cellular changes that culminate in clinical disease, occur in the very early years of life. Because it identifies babies at high risk for Beta-cell autoimmunity prior to their earliest production of autoantibodies, our neonatal genetic screening program provides us with our first chance ever to test the hypothesis in a cohort design.