Loss of immune tolerance to IL-2 in type 1 diabetes

Nat Commun. 2016 Oct 6:7:13027. doi: 10.1038/ncomms13027.

Abstract

Type 1 diabetes (T1D) is characterized by a chronic, progressive autoimmune attack against pancreas-specific antigens, effecting the destruction of insulin-producing β-cells. Here we show interleukin-2 (IL-2) is a non-pancreatic autoimmune target in T1D. Anti-IL-2 autoantibodies, as well as T cells specific for a single orthologous epitope of IL-2, are present in the peripheral blood of non-obese diabetic (NOD) mice and patients with T1D. In NOD mice, the generation of anti-IL-2 autoantibodies is genetically determined and their titre increases with age and disease onset. In T1D patients, circulating IgG memory B cells specific for IL-2 or insulin are present at similar frequencies. Anti-IL-2 autoantibodies cloned from T1D patients demonstrate clonality, a high degree of somatic hypermutation and nanomolar affinities, indicating a germinal centre origin and underscoring the synergy between cognate autoreactive T and B cells leading to defective immune tolerance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Animals
  • Autoantibodies / immunology
  • Diabetes Mellitus, Type 1 / immunology*
  • Epitopes / immunology
  • Female
  • Humans
  • Immune Tolerance*
  • Immunoglobulin G / immunology
  • Interleukin-2 / immunology*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Inbred NOD
  • Middle Aged
  • Pancreas / immunology
  • Peptides / immunology
  • T-Lymphocytes / cytology
  • Young Adult

Substances

  • Autoantibodies
  • Epitopes
  • IL2 protein, human
  • Immunoglobulin G
  • Interleukin-2
  • Peptides

Grants and funding