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

新开展的 1 型糖尿病霉酚酸酯-达利珠单抗临床试验

• 批准号: 7717081
• 负责人: DESMOND Arthur SCHATZ
• 金额: $ 4.55万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-12-01 至 2008-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7717081
• 关键词: Adverse effects; Autoantibodies; Autoimmune Process; Beta Cell; Biological Preservation; C-Peptide; Caring; Clinical Trials; Complications of Diabetes Mellitus; Computer Retrieval of Information on Scientific Projects Database; Daclizumab; Data; Diabetes Mellitus; Disease; Funding; Generations; Grant; Hypoglycemia; Immune; Immune response; Immune system; Immunologic Markers; Immunosuppression; Institution; Insulin; Insulin-Dependent Diabetes Mellitus; Intervention; Intervention Trial; Metabolic Control; Outcome; Production; Research; Research Personnel; Resources; Source; Surrogate Markers; T-Lymphocyte; Therapeutic immunosuppression; Time; United States National Institutes of Health; Work; base; cost; diabetic; immunoregulation; improved; islet; mycophenolate mofetil; outcome forecast; prevent; response

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.

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， 因此可以在其他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。 本研究旨在确定免疫干预策略，以防止1型糖尿病发病时β细胞破坏的进展。一些β细胞的持续存在应该改善长期糖尿病护理，预防疾病本身的并发症，但也预防低血糖，这是其管理的结果。目的是阻止新糖尿病受试者中的β细胞破坏，因为一旦自身免疫过程已经进展到β细胞的完全或接近完全破坏，免疫调节可能无法单独良好地起作用。书房？的基本原理是证明在这项研究的4年过程中，胰岛功能的保护和最小的免疫系统副作用。 如果结果足够积极，这项临床试验的数据可以作为更大规模试验的基础，或者它们可以建议其他联合干预试验，这些试验可能会获得更好的疗效或可能保留C肽，而不需要继续进行免疫抑制。 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。干预，可以恢复正常的胰岛功能和维持胰岛素的生产将显着改善糖尿病代谢控制的预后，从而减少长期并发症。 本研究还将检查所提出的治疗对免疫学效应和免疫学结果的替代标志物的影响。免疫应答的调节可以降低自身抗体滴度，并减少或防止自身抗原性T细胞应答的产生。