Transactivation by AP-1 is a molecular target of T cell clonal anergy

Science. 1992 Aug 21;257(5073):1134-8. doi: 10.1126/science.257.5073.1134.

Abstract

Anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. Anergic T cells were shown to have a defect in antigen-induced transcription of the interleukin-2 gene. Analysis of the promoter indicated that the transcription factor AP-1 and its corresponding cis element were specifically down-regulated. Exposure of anergic T cells to interleukin-2 restored both antigen responsiveness and activity of the AP-1 element.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigen-Presenting Cells / immunology
  • Antigens / immunology*
  • Base Sequence
  • Binding Sites
  • Blotting, Northern
  • Cell Line
  • Concanavalin A / pharmacology
  • Gene Expression Regulation*
  • Immune Tolerance*
  • Interleukin-2 / genetics*
  • Interleukin-2 / pharmacology
  • Mice
  • Molecular Sequence Data
  • Mutation
  • Promoter Regions, Genetic / genetics
  • Proto-Oncogene Proteins c-jun / physiology*
  • RNA, Messenger / metabolism
  • Receptors, Antigen, T-Cell / immunology
  • T-Lymphocytes / immunology*
  • Transcription, Genetic
  • Transfection

Substances

  • Antigens
  • Interleukin-2
  • Proto-Oncogene Proteins c-jun
  • RNA, Messenger
  • Receptors, Antigen, T-Cell
  • Concanavalin A