NLM Gateway
A service of the U.S. National Institutes of Health
Your Entrance to
Resources from the
National Library of Medicine
    Home      Term Finder      Limits/Settings      Search Details      History      My Locker        About      Help      FAQ    
Skip Navigation Side Barintended for web crawlers only

Single cell analysis of lymphokine imbalance in asymptomatic HIV1 infection: evidence for a major alteration within the CD8+ T cell subset.

Victorino RM, Sousa AE; Keystone Symposia on Molecular and Cellular Biology: 1998 HIV Pathogenesis and Treatment.

Keyst Symp Mol Cell Biol Keyst Symp Mol Cell Biol. 1998 Mar 13-19; 104 (abstract no. 4093).

Faculty of Medicine of Lisbon-Cellular Immunology Unit (CEBIP), Lisbon, Portugal.

In this study we investigated at single cell level by flow cytometry the potential of T cell cytokine production in asymptomatic HIV1 infected subjects with more than 200 CD4 counts and possible correlation with T helper cell depletion and viral load. Mitogen stimulated peripheral blood mononuclear cells from 32 HIV1+ patients and 16 healthy subjects were intracytoplasmicaly stained for IL2, IFNgamma, IL4 or IL10, and the frequency of cytokine producing cells was assessed in total T cells, CD4, CD8, CD28 and CD45RO subsets as well as in CD69+CD3+ gated lymphocytes. HIV1+ patients, irrespectively of their degree of CD4 depletion, exhibited a major increase in IFNgamma+ CD8 T cells, largely due to CD28- cells, as well as a decrease in the capacity of CD8 T cells to produce IL2. Patients with more than 500 CD4 counts showed a diminished frequency of IL4 expression in CD4 T cells and a negative correlation was found between this parameter and the ex vivo CD4 counts in the 32 patients. Analysis of patients stratified according to viral load revealed a significantly higher proportion of IL2 producing CD4 cells in the group with less than 5000 RNA copies/ml. In summary, using single cell analysis and an APC independent stimulus, we have not been able to find major cytokine imbalances in the CD4 subset, suggesting that the well described T helper defects are not due to intrinsic alterations in the potential of CD4 T cells to produce cytokines. On the other hand, the major disturbances in the CD8 T lymphocytes agrees with the marked activation and possible replicative senescence of CD8 T cells and emphasises the role of this subset in HIV immunopathogenesis.

Publication Types:
  • Meeting Abstracts
Keywords:
  • Antigens, CD
  • Antigens, CD28
  • Antigens, CD3
  • Antigens, CD4
  • Antigens, CD45
  • Antigens, CD8
  • CD4 Lymphocyte Count
  • CD4-Positive T-Lymphocytes
  • CD69 antigen
  • CD8-Positive T-Lymphocytes
  • Communicable Diseases
  • Cytokines
  • HIV Infections
  • HIV Seropositivity
  • HIV-1
  • Humans
  • Interleukin-2
  • Interleukin-4
  • Lymphokines
  • T-Lymphocyte Subsets
  • T-Lymphocytes
  • T-Lymphocytes, Helper-Inducer
  • Viral Load
  • immunology
Other ID:
  • 98930516
UI: 102236944

From Meeting Abstracts




Contact Us
U.S. National Library of Medicine |  National Institutes of Health |  Health & Human Services
Privacy |  Copyright |  Accessibility |  Freedom of Information Act |  USA.gov