Class-switched anti-insulin antibodies originate from unconventional antigen presentation in multiple lymphoid sites

J Exp Med. 2016 May 30;213(6):967-78. doi: 10.1084/jem.20151869. Epub 2016 May 2.

Abstract

Autoantibodies to insulin are a harbinger of autoimmunity in type 1 diabetes in humans and in non-obese diabetic mice. To understand the genesis of these autoantibodies, we investigated the interactions of insulin-specific T and B lymphocytes using T cell and B cell receptor transgenic mice. We found spontaneous anti-insulin germinal center (GC) formation throughout lymphoid tissues with GC B cells binding insulin. Moreover, because of the nature of the insulin epitope recognized by the T cells, it was evident that GC B cells presented a broader repertoire of insulin epitopes. Such broader recognition was reproduced by activating naive B cells ex vivo with a combination of CD40 ligand and interleukin 4. Thus, insulin immunoreactivity extends beyond the pancreatic lymph node-islets of Langerhans axis and indicates that circulating insulin, despite its very low levels, can have an influence on diabetogenesis.

Publication types

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

MeSH terms

  • Animals
  • Antigen Presentation / genetics
  • Antigen Presentation / immunology*
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / pathology
  • CD40 Antigens / genetics
  • CD40 Antigens / immunology
  • Diabetes Mellitus, Type 1 / genetics
  • Diabetes Mellitus, Type 1 / immunology*
  • Diabetes Mellitus, Type 1 / pathology
  • Germinal Center / immunology*
  • Germinal Center / pathology
  • Immunoglobulin Class Switching / genetics
  • Immunoglobulin Class Switching / immunology*
  • Insulin / genetics
  • Insulin / immunology*
  • Interleukin-4 / genetics
  • Interleukin-4 / immunology
  • Islets of Langerhans / immunology
  • Islets of Langerhans / pathology
  • Mice
  • Mice, Knockout
  • T-Lymphocytes / immunology
  • T-Lymphocytes / pathology

Substances

  • CD40 Antigens
  • Insulin
  • Interleukin-4