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Abstract
Importance of the field: Type 1 diabetes mellitus (T1D) is a T-cell mediated autoimmune disease with selective destruction of β cells. Immunological interventions are directed at arresting the loss of β-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 β-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 β-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 β-cell function.