Cutting edge: Enhanced IL-2 signaling can convert self-specific T cell response from tolerance to autoimmunity

J Immunol. 2008 May 1;180(9):5789-93. doi: 10.4049/jimmunol.180.9.5789.

Abstract

Naive and memory T cells show differences in their response to antigenic stimulation. We examined whether this difference extended to the peripheral deletion of T cells reactive to self-Ag or, alternatively, the induction of autoimmunity. Our results show that although both populations where susceptible to deletion, memory T cells, but not naive T cells, also gave rise to autoimmunity after in vivo presentation of skin-derived self-Ags. The same migratory dendritic cells presented self-Ag to both naive and memory T cell populations, but only the latter had significant levels of the effector molecule granzyme B. Memory T cells also expressed increased levels of the high affinity IL-2 receptor chain after self-Ag recognition. Provision of IL-2 signaling using a stimulatory complex of anti-IL-2 Ab and IL-2 drove the otherwise tolerant naive T cells toward an autoimmune response. Therefore, enhanced IL-2 signaling can act as a major selector between tolerance and autoimmunity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigen Presentation / physiology
  • Autoantigens / immunology*
  • Autoimmunity / physiology*
  • Cell Movement / immunology
  • Dendritic Cells / cytology
  • Dendritic Cells / immunology
  • Granzymes / immunology
  • Immune Tolerance / physiology*
  • Immunologic Memory / physiology
  • Interleukin-2 / immunology*
  • Mice
  • Receptors, Interleukin-2 / immunology
  • Signal Transduction
  • Skin / cytology
  • Skin / immunology*
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology*

Substances

  • Autoantigens
  • Interleukin-2
  • Receptors, Interleukin-2
  • Granzymes
  • Gzmb protein, mouse