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- Title
Immunology: Insulin auto-antigenicity in type 1 diabetes.
- Authors
Wilson, Darcy B.
- Abstract
Arising from: M. Nakayama et al. 435, 220–223 (2005) and et al. 435, 224–228 (2005); D. A. Hafler et al. replySpontaneous type 1 diabetes occurs when the autoimmune destruction of pancreatic β-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 considered. Nakayama et al. and Kent et al. 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..
- Subjects
CELLS; DIABETES; T cells; INSULIN; IMMUNOLOGY; ANTIGENS; METABOLISM; HORMONES; GLUCOSE; LYMPHOCYTES
- Publication
Nature, 2005, Vol 438, Issue 7067, pE5
- ISSN
0028-0836
- Publication type
Article
- DOI
10.1038/nature04423