In The Lancet, Antoinette Moran, Linda Pickersgill, and their respective colleagues1 report the findings of two independent phase 2 randomised placebo-controlled clinical trials that assessed the efficacy of interleukin-lp inhibition as a means to halt deterioration of (3-cell function after the onset of type 1 diabetes. Type 1 diabetes results from immune-mediated (3-cell loss.2 Interfering with theT-lymphocyte or B-lymphocyte arms of the adaptive immune system transiently stabilises (3-cell function.35 Thus, targeting the other major weaponry of the immune system, innate immunity, by inhibition of what is regarded as one of its main regulators, interleukin-lp, would seem appropriate. The two trials were undertaken in the USA and Canada, and Europe, respectively. In the trial in the USA and Canada, patients with recent-onset type 1 diabetes were randomly assigned to receive the human monoclonal anti-interleukin-ip antibody canakinumab (n=47) or placebo (n=22). In the European trial, patients were randomly assigned to receive the human interleukin-1 receptor antagonist anakinra (n=35) or placebo (n=34)-Both drugs have been successfully used to treat other autoimmune diseases, such as rheumatoid arthritis.6'7 Anakinra was also efficacious in type 2 diabetes.8
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