Lymphocyte activation gene-3 expression defines a discrete subset of HIV-Specific CD8+ T cells that is associated with Lower Viral Load

José Peña, Norman G. Jones, Stephanie Bousheri, David R. Bangsberg, Huyen Cao

Research output: Contribution to journalArticle

10 Scopus citations


Mechanisms leading to the observed immune dysregulation in chronic HIV infection are not well understood. The MHC-II class ligand, lymphocyte activation gene-3 (LAG-3, CD223), has been implicated in the complex regulation mechanism of immune functions. In this study, we describe a new population of HIV-specific CD8+ T cells expressing LAG-3. These LAG-3 +CD8+ T cells do not display immunophenotypic patterns traditionally attributed to regulatory T cells. The LAG3+CD8 + T cells are CCR7+,CD127-, and display heterogeneous surface expressions of CD45RA and CD25. Interestingly, HIV-specific LAG-3+CD8+ T cells do not substantially express CTLA-4 and LAG-3 expression does not correlate with interleukin (IL)-10 or tumor growth factor (TGF)-β production. In addition, HIV-specific LAG3+CD8+ T cells do not produce interferon (IFN-γ) or express CD107a. The frequency of HIV-specific LAG3+CD8+ T cells negative correlated with plasma viral load. Our study introduces a new population of HIV-specific CD8+ T cells and proposes additional mechanisms of immune regulation in chronic HIV infection.

Original languageEnglish (US)
Pages (from-to)535-541
Number of pages7
JournalAIDS Research and Human Retroviruses
Issue number6
StatePublished - Jun 1 2014


ASJC Scopus subject areas

  • Immunology
  • Virology
  • Infectious Diseases

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