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

Overview

abstract

  • CD1d-restricted NKT cells express an invariant TCR and have been demonstrated to play an important regulatory role in a variety of immune responses. Invariant NKT cells down-regulate autoimmune responses by production of type 2 cytokines and can initiate antitumor and antimicrobial immune responses by production of type 1 cytokines. Although defects in the (invariant) Valpha24+Vbeta11+ NKT cell population have been observed in patients with cancer and autoimmune diseases, little is known regarding the protective role of Valpha24+Vbeta11+ NKT cells in human infectious disease. In a cross-sectional study in HIV-1-infected individuals, we found circulating numbers of Valpha24+Vbeta11+ NKT cells to be reduced, independent of CD4+ T cell counts, CD4:CD8 ratios, and viral load. Because a small minority of Valpha24+Vbeta11+ NKT cells of healthy donors expressed HIV-1 (co)receptors and the vast majority of Valpha24+Vbeta11+ NKT cells in HIV-1-infected individuals expressed the Fas receptor, the depletion was more likely due to Fas-mediated apoptosis than to preferential infection of Valpha24+Vbeta11+ NKT cells by HIV-1. A longitudinal cohort study, in which patients were analyzed before seroconversion and 1 and 5 years after seroconversion, demonstrated that a large proportion of the depletion occurred within the first year postseroconversion. In this longitudinal study no evidence was found to support an important role of Valpha24+Vbeta11+ NKT cells in determining the rate of progression during HIV-1 infection.

publication date

  • February 1, 2002

Research

keywords

  • HIV Infections
  • HIV-1
  • Killer Cells, Natural
  • Receptors, Antigen, T-Cell, alpha-beta
  • T-Lymphocyte Subsets

Identity

Scopus Document Identifier

  • 0036467364

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.168.3.1490

PubMed ID

  • 11801694

Additional Document Info

volume

  • 168

issue

  • 3