NEW ONSET OF TYPE 1 DIABETES MYCOPHENOLATE MOFETIL-DACLIZUMAB CLINICAL TRIAL

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 这项研究是为了确定免疫干预策略，以防止从1型糖尿病发病时起β细胞破坏的进展。一些β细胞的持续存在应该会改善长期的糖尿病护理，防止疾病本身的并发症，但也会预防低血糖，这是其管理的结果。其目的是阻止新糖尿病患者的β细胞破坏，因为一旦自身免疫过程进展到完全或接近完全破坏β细胞，免疫调节可能不会很好地发挥作用。S的这项研究的基本原理是在4年的研究过程中证明在免疫系统副作用最小的情况下保存胰岛功能。 如果结果足够积极，来自这项临床试验的数据可以作为更大规模试验的基础，或者它们可以建议进行其他联合干预试验，这些试验可能取得更好的疗效，或者可能在不需要持续免疫抑制的情况下保留C肽。 长期糖尿病的并发症和成本是众所周知的，目前糖尿病并发症的成本每年超过1000亿美元。能够恢复正常胰岛功能和维持胰岛素产生的干预措施将显著改善糖尿病代谢控制的预后，从而减少长期并发症。 这项研究还将检验拟议的治疗方法对免疫效果和免疫结果的替代标记物的影响。调节免疫反应可以降低自身抗体效价，减少或防止自身抗原T细胞反应的产生。

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. This study is to identify immune intervention strategies that will prevent the progression of beta cell destruction from the time of onset of type 1 diabetes. The persistence of some beta cells should improve long-term diabetes care and prevent complications of the disease itself but also hypoglycemia, which is a consequence of its management. The aim is to arrest beta cell destruction in newly diabetic subjects because immune modulation may not work well alone once the autoimmune process has progressed to complete or near complete destruction of beta cells. The study?s rationale is to demonstrate a preservation of islet function with minimal immune system side effects over the 4-year course of this study. The data from this clinical trial could serve as the basis for a larger trial if the results are sufficiently positive, or they could suggest other combined intervention trials that might achieve either better efficacy or potentially preserve C-peptide without the need for continued immunosuppression. The complications and costs of long-term diabetes are well known and the costs of diabetes complications are currently greater than $100 billion a year. An intervention, which could restore normal islet function and maintain production of insulin would significantly improve the prognosis for metabolic control of diabetes and thus reduce long-term complications. This study will also examine the effect of the proposed treatment on surrogate markers for immunologic effects and immunological outcomes Modulation of the immune response could lower autoantibody titers and either reduce or prevent the generation of autoantigenic T-cell responses.