INTRODUCTION: Type 1 diabetes is an organ-specific autoimmune disease, 
characterized by selective destruction of insulin-producing pancreatic β-cells 
by T-cell-mediated inflammation. Beginning with studies of cyclosporin A in the 
1980s, but with more activity in the past decade, there have been a number of 
clinical trials to test whether immunotherapies can arrest the decline in 
C-peptide, which is associated with progression of type 1 diabetes leading to 
the metabolic instability that characterizes the disease. One of the most 
promising agents, teplizumab , is an FcR-nonbinding anti-CD3 monoclonal antibody 
that has been tested in Phase II - III clinical trials and was shown to preserve 
the C-peptide levels and reduce the need for exogenous insulin.
AREAS COVERED: In this review, we discuss the recent update on clinical data 
obtained from trials of teplizumab in type 1 diabetes, the drug's postulated 
mechanism of action and the identification of responders to therapy. We 
highlight the results of recent trials as well as the lessons that have been 
learned from the clinical trials involving selection of end points and the 
inclusion of diverse study populations.
EXPERT OPINION: Teplizumab has been shown to preserve β cell function in 
patients; however, it does not represent a 'cure' for patients, and its efficacy 
does entail a significant advance in arresting the progression of the disease 
toward complete insulin deficiency and reliance on exogenous insulin.