Skip to main content
  • Poster presentation
  • Open access
  • Published:

Increased PD-1 expression in cynomolgus and rhesus macaques during lentiviral infection

Costimulatory molecules play important roles in immunoregulation. Recent evidence in mice suggests programmed death-1 (PD-1) is a marker for T-cell exhaustion in a murine LCMV model. Here we demonstrate increased PD-1 expression in CD3+ T cells following lentiviral infection in cynomolgus and rhesus macaques with a concomitant increase in CD4+ CD8+ double-positive (DP) T cells. We found DP T cells are PD-1hi and demonstrate a high proliferative capacity in response to lectin stimulation. DP PD-1hi T-cell populations contain functionally active antigen-specific T cells, secreting IFN-γ and expressing CD107a upon stimulation using Gag peptide pools. Finally, we report an inverse correlation between PD-1 expression on CD4 single-positive T cells and CD4+ T-cell counts. Our data indicate PD-1 as a possible marker for immune health during lentiviral infection and suggest higher PD-1 expression in chronically infected monkeys is indicative of T-cell stimulation rather than T-cell exhaustion. To our knowledge, this is the first study of PD-1 expression in non-human primates.

Author information

Authors and Affiliations

Authors

Rights and permissions

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and permissions

About this article

Cite this article

Hokey, D.A., Boyer, J.D., Yoon, H. et al. Increased PD-1 expression in cynomolgus and rhesus macaques during lentiviral infection. Retrovirology 3 (Suppl 1), P27 (2006). https://doi.org/10.1186/1742-4690-3-S1-P27

Download citation

  • Published:

  • DOI: https://doi.org/10.1186/1742-4690-3-S1-P27

Keywords