Antigen presentation in the autoimmune diabetes of the NOD mouse

Annu Rev Immunol. 2014;32:579-608. doi: 10.1146/annurev-immunol-032712-095941. Epub 2014 Feb 5.

Abstract

This paper reviews the presentation of peptides by major histocompatibility complex (MHC) class II molecules in the autoimmune diabetes of the nonobese diabetic (NOD) mouse. Islets of Langerhans contain antigen-presenting cells that capture the proteins and peptides of the beta cells' secretory granules. Peptides bound to I-A(g7), the unique MHC class II molecule of NOD mice, are presented in islets and in pancreatic lymph nodes. The various beta cell-derived peptides interact with selected CD4 T cells to cause inflammation and beta cell demise. Many autoreactive T cells are found in NOD mice, but not all have a major role in the initiation of the autoimmune process. I emphasize here the evidence pointing to insulin autoreactivity as a seminal component in the diabetogenic process.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antigen Presentation / immunology*
  • Antigen-Presenting Cells / immunology
  • Autoantigens / immunology
  • Diabetes Mellitus, Type 1 / immunology*
  • Disease Models, Animal
  • Epitopes, T-Lymphocyte
  • Histocompatibility Antigens Class II / chemistry
  • Histocompatibility Antigens Class II / immunology
  • Humans
  • Insulin / immunology
  • Islets of Langerhans / cytology
  • Islets of Langerhans / immunology
  • Lymphocyte Activation / immunology
  • Mice
  • Mice, Inbred NOD
  • Peptides / immunology
  • T-Cell Antigen Receptor Specificity / immunology
  • T-Lymphocyte Subsets / immunology

Substances

  • Autoantigens
  • Epitopes, T-Lymphocyte
  • Histocompatibility Antigens Class II
  • Insulin
  • Peptides