Immunology: Insulin auto-antigenicity in type 1 diabetes

Nature. 2005 Nov 24;438(7067):E5; discussion E5-6. doi: 10.1038/nature04423.

Abstract

Spontaneous type 1 diabetes occurs when the autoimmune destruction of pancreatic beta-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..

Publication types

  • Comment

MeSH terms

  • Animals
  • Autoantigens / chemistry
  • Autoantigens / immunology*
  • Autoimmunity / immunology*
  • Cross Reactions
  • Diabetes Mellitus, Type 1 / immunology*
  • Disease Models, Animal
  • Humans
  • Insulin / chemistry
  • Insulin / immunology*
  • Insulin / metabolism
  • Insulin Secretion
  • Islets of Langerhans / immunology
  • Islets of Langerhans / metabolism
  • Islets of Langerhans / pathology
  • Lymph Nodes / cytology
  • Lymph Nodes / immunology
  • Mice
  • Models, Immunological*
  • Peptide Fragments / chemistry
  • Peptide Fragments / immunology
  • Reproducibility of Results
  • T-Lymphocytes / immunology*

Substances

  • Autoantigens
  • Insulin
  • Peptide Fragments