A regulatory role for TRAF1 in antigen-induced apoptosis of T cells

J Exp Med. 1997 May 19;185(10):1777-83. doi: 10.1084/jem.185.10.1777.

Abstract

Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) and TRAF1 were found as components of the TNFR2 signaling complex, which exerts multiple biological effects on cells such as cell proliferation, cytokine production, and cell death. In the TNFR2-mediated signaling pathways, TRAF2 works as a mediator for activation signals such as NF-kappaB, but the role of TRAF1 has not been previously determined. Here we show in transgenic mice that TRAF1 overexpression inhibits antigen-induced apoptosis of CD8(+) T lymphocytes. Our results demonstrate a biological role for TRAF1 as a regulator of apoptotic signals and also support the hypothesis that the combination of TRAF proteins in a given cell type determines distinct biological effects triggered by members of the TNF receptor superfamily.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens
  • Apoptosis*
  • CD8-Positive T-Lymphocytes / immunology
  • Cell Survival
  • Cytotoxicity, Immunologic
  • Lymph Nodes / immunology
  • Lymphocyte Activation
  • Macrophages / immunology
  • Mice
  • Mice, Transgenic
  • Proteins / genetics
  • Proteins / physiology*
  • Receptors, Antigen, T-Cell, alpha-beta / genetics
  • Receptors, Antigen, T-Cell, alpha-beta / physiology*
  • Receptors, Tumor Necrosis Factor / physiology
  • Recombinant Fusion Proteins / biosynthesis
  • Signal Transduction
  • Spleen / immunology
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / physiology*
  • TNF Receptor-Associated Factor 1
  • TNF Receptor-Associated Factor 2

Substances

  • Antigens
  • Proteins
  • Receptors, Antigen, T-Cell, alpha-beta
  • Receptors, Tumor Necrosis Factor
  • Recombinant Fusion Proteins
  • TNF Receptor-Associated Factor 1
  • TNF Receptor-Associated Factor 2