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: 7950709
• 负责人: DESMOND Arthur SCHATZ
• 金额: $ 0.95万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-12-01 至 2009-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7950709
• 关键词: Adverse effects; Autoantibodies; Autoimmune Diseases; Autoimmune Process; Beta Cell; Biological Preservation; C-Peptide; Caring; Chronic; Clinical Research; Clinical Trials; Computer Retrieval of Information on Scientific Projects Database; Daclizumab; Data; Diabetes Mellitus; Disease; Funding; Generations; Grant; Human; Hypoglycemia; Immune; Immune response; Immune system; Immunologics; Immunosuppression; Institution; Insulin; Insulin-Dependent Diabetes Mellitus; Intervention; Intervention Trial; Metabolic Control; Outcome; Production; Research; Research Personnel; Resources; Source; Surrogate Markers; T-Lymphocyte; Time; United States National Institutes of Health; Work; base; diabetic; immunoregulation; improved; insulin dependent diabetes mellitus onset; 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. The body of evidence developed over the last 10 - 20 years suggests that type 1 diabetes (T1D) in humans is a chronic, slowly progressive autoimmune disease. The objective of this study is to identify immune intervention strategies that will prevent the progression of beta cell destruction from the time of onset of T1D. The persistence of at least some beta cells should improve long-term diabetes care and prevent not only 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 meaningful preservation of islet function with minimal immune system side effects. 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. 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 outcomes Modulation of the immune response could lower autoantibody titers and either reduce or prevent the generation of autoantigenic T-cell responses.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 过去 10 - 20 年的大量证据表明，人类 1 型糖尿病 (T1D) 是一种慢性、缓慢进展的自身免疫性疾病。本研究的目的是确定免疫干预策略，以防止从 T1D 发病时起β细胞破坏的进展。至少一些β细胞的持续存在应该可以改善长期糖尿病护理，不仅可以预防疾病本身的并发症，还可以预防低血糖（这是其管理的结果）。其目的是阻止新发糖尿病受试者的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，单独的免疫调节可能无法很好地发挥作用。该研究的基本原理是证明胰岛功能的有意义的保存和最小的免疫系统副作用。 如果结果足够积极，该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，这些试验可能会实现更好的疗效或可能保留 C 肽，而无需持续免疫抑制。 能够恢复正常胰岛功能并维持胰岛素产生的干预措施将显着改善糖尿病代谢控制的预后，从而减少长期并发症。 这项研究还将检查所提议的治疗对免疫效应和结果的替代标记物的影响。免疫反应的调节可以降低自身抗体滴度，并减少或阻止自身抗原 T 细胞反应的产生。