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Related Experiment Videos

Selective decrease in circulating V alpha 24+V beta 11+ NKT cells during HIV type 1 infection.

Hans J J van der Vliet1, B Mary E von Blomberg, Mette D Hazenberg

  • 1Department of Medical Oncology, Pathology, and Internal Medicine, Free University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.

Journal of Immunology (Baltimore, Md. : 1950)
|January 22, 2002
PubMed
Summary

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Invariant NKT cells, crucial for immune regulation, are reduced in HIV-1 infection, primarily due to Fas-mediated apoptosis, not direct viral infection. Their numbers decline rapidly post-seroconversion but don't predict disease progression.

Area of Science:

  • Immunology
  • Virology
  • Cellular Biology

Background:

  • CD1d-restricted NKT cells, expressing invariant TCR, regulate immune responses via type 1 and type 2 cytokines.
  • These cells are implicated in autoimmune, antitumor, and antimicrobial immunity.
  • Defects in Valpha24+Vbeta11+ NKT cells are noted in cancer and autoimmune diseases, but their role in infectious diseases is unclear.

Purpose of the Study:

  • To investigate the role and dynamics of Valpha24+Vbeta11+ NKT cells in HIV-1 infection.
  • To determine the mechanisms behind NKT cell depletion in HIV-1-infected individuals.
  • To assess the association between NKT cell numbers and HIV-1 disease progression.

Main Methods:

  • Cross-sectional study of HIV-1-infected individuals.

Related Experiment Videos

  • Longitudinal cohort study analyzing patients before and after seroconversion (1 and 5 years).
  • Flow cytometry to assess NKT cell populations, HIV-1 (co)receptor expression, and Fas receptor expression.
  • Main Results:

    • Circulating Valpha24+Vbeta11+ NKT cells were reduced in HIV-1-infected individuals, irrespective of CD4 counts, CD4:CD8 ratios, or viral load.
    • Depletion was attributed to Fas-mediated apoptosis, as most NKT cells in infected individuals expressed Fas receptor.
    • A significant proportion of NKT cell depletion occurred within the first year post-seroconversion.
    • No evidence linked NKT cell numbers to the rate of HIV-1 disease progression.

    Conclusions:

    • HIV-1 infection leads to a significant reduction in Valpha24+Vbeta11+ NKT cells, primarily through Fas-mediated apoptosis.
    • The depletion occurs early in infection, within the first year post-seroconversion.
    • Invariant NKT cells do not appear to play a major role in determining the progression rate of HIV-1 infection.