FOXP3 expressing CD127lo CD4+ T cells inversely correlate with CD38+ CD8+ T cell activation levels in primary HIV-1 infection. Academic Article uri icon

Overview

abstract

  • During the course of HIV-1 infection, the status of immune activation has been determined to be a powerful indicator of disease progression. The immune system has adopted self-regulatory mechanisms to counterbalance undesirable immune responses. CD25+CD4+ T regulatory (Treg) cells that express the transcription regulator, forkhead box P3 (FOXP3), play an important role in this immunosuppression. Using a combination of Treg cell discriminatory markers (FOXP3, CD25, CD127), we predicted that an expansion of Treg cell subsets would negatively correlate with immune activation during the early stages of HIV-1 infection. We report that FOXP3+CD127lo expressing CD4+ T cells increases in primary HIV-1 infection over time. Furthermore, the FOXP3+CD127lo CD4+ T cells may, in fact, reduce the levels of T cell activation following primary infection. It is interesting that the positive correlation between FOXP3+CD127lo CD4+ and CD25+CD127lo CD4+ T cells noted in HIV-uninfected persons is not only lost but may also be reversed in early, chronic HIV-1 infection. Unlike FOXP3+CD127lo CD4+, the level of FOXP3+CD25+CD127lo CD4+ T cells did not correlate with T cell activation, suggesting that these cells were not effective in reducing T cell activation. These observations suggest that different Treg populations may have different effects on reducing immune activation in HIV-1 infection and that the FOXP3+CD127lo CD4+ T cell population may be particularly important in limiting immune activation.

publication date

  • November 2, 2007

Research

keywords

  • ADP-ribosyl Cyclase 1
  • CD8-Positive T-Lymphocytes
  • Forkhead Transcription Factors
  • HIV Infections
  • HIV-1
  • Interleukin-7 Receptor alpha Subunit
  • Membrane Glycoproteins
  • T-Lymphocyte Subsets
  • T-Lymphocytes, Regulatory

Identity

Scopus Document Identifier

  • 38949128315

Digital Object Identifier (DOI)

  • 10.1189/jlb.0507281

PubMed ID

  • 17982112

Additional Document Info

volume

  • 83

issue

  • 2