Abstract

Arising from: M. Nakayama et al. Nature 435, 220–223 (2005) and S. C. Kent et al. Nature 435, 224–228 (2005); D. A. Hafler et al. reply

Spontaneous type 1 diabetes occurs when the autoimmune destruction of pancreatic -islet cells prevents production of the hormone insulin. This causes an inability to regulate glucose metabolism, which results in dangerously raised blood glucose concentrations. It is generally accepted that thymus-derived lymphocytes (T cells) are critically involved in the onset and progression of type 1 diabetes, but the antigens that initiate and drive this destructive process remain poorly characterized — although several candidates have been considered¹. Nakayama et al.² and Kent et al.³ claim that insulin itself is the primary autoantigen that initiates spontaneous type 1 diabetes in mice and humans, respectively, a result that could have implications for more effective prevention and therapy. However, I believe that this proposed immunological role of insulin may be undermined by the atypical responses of T cells to the human insulin fragment that are described by Kent et al.³.

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