The matrix protein pp65(341-350): a peptide that induces ex vivo stimulation and in vitro expansion of CMV-specific CD8+ T cells in subjects bearing either HLA-A*2402 or A*0101 allele

Transfusion. 2003 Nov;43(11):1567-74. doi: 10.1046/j.1537-2995.2003.00564.x.

Abstract

Background: The stimulation of PBMNCs with HLA Class I restricted synthetic peptides derived from CMV phosphorylated matrix protein 65 (pp65) evokes CMV-specific cytotoxic T lymphocyte (CTL) activity, a necessary condition for initiating adoptive immunotherapy against CMV-related diseases in immune-compromised patients. It was previously demonstrated that the CMV decamer (10-mer) peptide pp65(341-350), QYDPVAALFF, was able to induce CMV-specific CTLs in HLA-A*2402 CMV-seropositive individuals.

Study design and method: We investigated the ability of the peptide pp65(341-350) to reactivate memory CD8+ T cells in CMV-seropositive subjects bearing either the HLA-A24 or A1 allele. CTL responses were measured by IFN-gamma mRNA expression and IFN-gamma protein production as well as cytotoxic activity.

Results: In this study it was found that peptide pp65(341-350) induced a specific reactivation of memory CD8+ T cells from CMV-seropositive donors expressing either HLA-A*2402 and/or HLA-A*0101. Moreover, a pp65(341-350)-specific selection and expansion using PBMNCs of CMV-seropositive donors bearing both HLA-A*2402 and HLA-A*0101 alleles produced cytotoxic CTLs to both HLA-A24 and A1 peptide-pulsed and autologous CMV-infected target cells.

Conclusion: The results demonstrate that pp65(341-350) induced a specific CTL activity at both molecular and protein levels and that the peptide is specifically processed, presented, and recognized by subjects bearing HLA-A*2402 and/or A*0101. These findings suggest that it may be possible to use this single immune dominant peptide to induce and expand CMV-reactive CTLs for the treatment of individuals with both HLA-A24 and A1 types.

MeSH terms

  • Alleles
  • CD8-Positive T-Lymphocytes / immunology*
  • CD8-Positive T-Lymphocytes / pathology*
  • Cell Death
  • Cell Division / drug effects
  • Cells, Cultured
  • Cytomegalovirus / immunology*
  • Cytomegalovirus Infections / blood
  • Cytotoxicity, Immunologic
  • HLA-A Antigens / genetics*
  • Humans
  • Interferon-gamma / genetics
  • Interferon-gamma / metabolism
  • Monocytes / metabolism
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology
  • Phosphoproteins / metabolism*
  • Phosphoproteins / pharmacology*
  • RNA, Messenger / biosynthesis
  • Viral Matrix Proteins / metabolism*
  • Viral Matrix Proteins / pharmacology*

Substances

  • HLA-A Antigens
  • Peptide Fragments
  • Phosphoproteins
  • RNA, Messenger
  • Viral Matrix Proteins
  • cytomegalovirus matrix protein 65kDa
  • Interferon-gamma