Teplizumab therapy for type 1 diabetes

被引:24
作者
Masharani, Umesh B. [1 ]
Becker, Joseph [1 ]
机构
[1] Univ Calif San Francisco, Dept Med, Div Endocrinol & Metab, San Francisco, CA 94143 USA
关键词
anti-CD3; antibody; immunologic tolerance; regulatory T cells; teplizumab; type; 1; diabetes; ANTI-CD3; MONOCLONAL-ANTIBODY; BONE-MARROW-TRANSPLANTATION; CYTOKINE-RELATED SYNDROME; TUMOR-NECROSIS-FACTOR; REGULATORY T-CELLS; IN-VIVO; RECENT-ONSET; NOD MICE; IMMUNOSUPPRESSIVE PROPERTIES; SELF-TOLERANCE;
D O I
10.1517/14712591003598843
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Importance of the field. 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. Areas covered in this review. 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. What the reader will gain: A broad perspective on the use of teplizumab in inducing disease specific tolerance. Take home message: 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.
引用
收藏
页码:459 / 465
页数:7
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