Late signals from CD27 prevent Fas-dependent apoptosis of primary CD8+ T cells

J Immunol. 2008 Mar 1;180(5):2912-21. doi: 10.4049/jimmunol.180.5.2912.

Abstract

The role of costimulation has previously been confined to the very early stages of the CD8+ T cell response. In this study, we demonstrate the requirement for CD27 costimulation during the later phase, but not programming of the primary CD8+ T cell response to influenza virus and reveal a novel mechanism of action for CD27 costimulation. CD27 signals, during the later phase of the primary CD8+ T cell response, prevent apoptosis of Ag-specific CD8+ T cells. Blocking CD27L (CD70) on days 6 and 8 after infection reduces the number of NP(366-374)-specific CD8+ T cells, increases their sensitivity to CD95/Fas-mediated apoptosis, and up-regulates FasL on CD4+ T cells. This reduction of NP(366-374)-specific CD8+ T cells requires the presence of CD4+ T cells and Fas signaling. Lack of CD27 signals also decreases the quality of memory CD8+ T cell responses. Memory CD8+ T cells, which express surface CD27 similar to naive cells, however, do not require CD27 costimulation during a secondary response. Thus, CD27 acts indirectly to regulate primary Ag-specific CD8+ T cell responses by preventing apoptosis of CD8+ T cells during the later phase of the primary response and is required for optimal quality of memory cells, but is not required during normally primed secondary CD8+ T cell responses.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adoptive Transfer
  • Animals
  • Antibodies, Blocking / metabolism
  • Antibodies, Monoclonal / metabolism
  • Apoptosis / genetics
  • Apoptosis / immunology*
  • CD27 Ligand / antagonists & inhibitors
  • CD27 Ligand / immunology
  • CD27 Ligand / metabolism
  • CD8-Positive T-Lymphocytes / immunology*
  • CD8-Positive T-Lymphocytes / metabolism*
  • CD8-Positive T-Lymphocytes / transplantation
  • CD8-Positive T-Lymphocytes / virology
  • Immunization, Secondary
  • Immunologic Memory / genetics
  • Influenza A virus / immunology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Orthomyxoviridae Infections / immunology
  • Orthomyxoviridae Infections / metabolism
  • Orthomyxoviridae Infections / virology
  • Peptide Fragments / administration & dosage
  • Peptide Fragments / immunology
  • Signal Transduction / genetics
  • Signal Transduction / immunology*
  • Time Factors
  • Tumor Necrosis Factor Receptor Superfamily, Member 7 / deficiency
  • Tumor Necrosis Factor Receptor Superfamily, Member 7 / genetics
  • Tumor Necrosis Factor Receptor Superfamily, Member 7 / metabolism
  • Tumor Necrosis Factor Receptor Superfamily, Member 7 / physiology*
  • Viral Core Proteins / administration & dosage
  • Viral Core Proteins / immunology
  • fas Receptor / biosynthesis
  • fas Receptor / deficiency
  • fas Receptor / genetics
  • fas Receptor / physiology*

Substances

  • Antibodies, Blocking
  • Antibodies, Monoclonal
  • CD27 Ligand
  • Cd70 protein, mouse
  • Peptide Fragments
  • Tumor Necrosis Factor Receptor Superfamily, Member 7
  • Viral Core Proteins
  • fas Receptor
  • nucleoprotein (366-374), influenza virus