Division of Endocrinology and Metabolism, Department of Medicine, University of California-San Francisco, 400 Parnassus Avenue, San Francisco, CA 94143, USA.
Expert Opin Biol Ther. 2010 Mar;10(3):459-65. doi: 10.1517/14712591003598843.
Type 1 diabetes mellitus (T1D) is a T-cell mediated autoimmune disease with selective destruction of beta cells. Immunological interventions are directed at arresting the loss of beta-cell function with the promise that this will make it easier for patients to control their glucose levels.
This review provides a summary of the preclinical and clinical research published between 1992 and 2009 using teplizumab and other anti-CD3 antibodies to arrest the loss of beta-cell function in new onset T1D. Data from animal and human studies on the probable mechanism of action of teplizumab are also reviewed.
A broad perspective on the use of teplizumab in inducing disease specific tolerance.
In Phase I/II randomized control trials, in patients with new onset T1D, teplizumab slowed the rate of loss of beta-cell function over 2 years of follow-up. Treated patients had better glycemic control and lower insulin requirements. Adverse events so far are mild and of limited duration. Phase III clinical trials are underway to confirm these results and to determine if two courses of drug have greater efficacy in arresting loss of beta-cell function.
1 型糖尿病（T1D）是一种 T 细胞介导的自身免疫性疾病，具有选择性破坏β细胞的特性。免疫干预的目的是阻止β细胞功能的丧失，以期使患者更容易控制血糖水平。
这篇综述提供了 1992 年至 2009 年期间使用替普单抗和其他抗 CD3 抗体的临床前和临床研究的总结，以阻止新诊断的 T1D 中β细胞功能的丧失。还回顾了关于替普单抗可能作用机制的动物和人体研究数据。
对替普单抗诱导疾病特异性耐受的广泛了解。
在 I/II 期随机对照试验中，在新诊断的 T1D 患者中，替普单抗在 2 年的随访中减缓了β细胞功能丧失的速度。接受治疗的患者血糖控制更好，胰岛素需求更低。到目前为止，不良事件轻微且持续时间有限。正在进行 III 期临床试验以确认这些结果，并确定两疗程药物是否更能有效阻止β细胞功能丧失。
