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: 7605456
• 负责人: DESMOND Arthur SCHATZ
• 金额: $ 9.65万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-12-23 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7605456
• 关键词: Adverse effects; Autoantibodies; Autoimmune Diseases; Autoimmune Process; Beta Cell; Biological Preservation; C-Peptide; Caring; Chronic; Clinical Trials; Complications of Diabetes Mellitus; Computer Retrieval of Information on Scientific Projects Database; Daclizumab; Data; Diabetes Mellitus; Disease; Funding; Generations; Grant; Human; 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; Adverse effects; Autoantibodies; Autoimmune Diseases; Autoimmune Process; Beta Cell; Biological Preservation; C-Peptide; Caring; Chronic; Clinical Trials; Complications of Diabetes Mellitus; Computer Retrieval of Information on Scientific Projects Database; Daclizumab; Data; Diabetes Mellitus; Disease; Funding; Generations; Grant; Human; 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. The great body of evidence developed over the last 10 - 20 years suggests that type 1 diabetes 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 type 1 diabetes. 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 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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 在过去的10到20年中，有大量证据表明，人类中的1型糖尿病是一种慢性，缓慢进行的自身免疫性疾病。这项研究的目的是确定免疫干预策略，以防止β细胞破坏从1型糖尿病发作开始。至少某些β细胞的持久性应改善长期糖尿病的护理，不仅可以预防疾病本身的并发症，而且还可以防止低血糖的并发症，这是其管理的结果。目的是阻止新的糖尿病患者中的β细胞破坏，因为一旦自身免疫性过程已完成或接近β细胞的完全破坏，免疫调节可能就无法单独使用。该研究的理由是在本研究的4年过程中证明对胰岛功能的有意义保存，具有最小的免疫系统副作用。 如果结果足够阳性，则该临床试验的数据可以作为更大试验的基础，或者他们可以提出其他合并的干预试验，这些试验可能会达到更好的疗效或潜在地保留C肽而无需持续免疫抑制。 长期糖尿病的并发症和成本众所周知，糖尿病并发症的成本目前每年大于1000亿美元。一种可以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。 这项研究还将检查拟议治疗对替代标记的影响，对免疫反应的免疫作用和免疫结果调节可能会降低自身抗体滴度，并减少或阻止自身抗原T细胞反应的产生。