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24+V
11+ NKT Cells During HIV Type 1 Infection1
Departments of
*
Medical Oncology,
Pathology, and
Internal Medicine, Free University Medical Center, Amsterdam, The Netherlands;
Department of Clinical Viro-Immunology, CLB, and the Laboratory for Experimental and Clinical Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and
¶ Cluster of Infectious Diseases, Municipal Health Service, Amsterdam, The Netherlands
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)
V
24+V
11+ NKT cell population have been
observed in patients with cancer and autoimmune diseases, little is
known regarding the protective role of
V24+V11+ NKT cells in human infectious
disease. In a cross-sectional study in HIV-1-infected individuals, we
found circulating numbers of V24+V11+ NKT
cells to be reduced, independent of CD4+ T cell counts,
CD4:CD8 ratios, and viral load. Because a small minority of
V24+V11+ NKT cells of healthy donors
expressed HIV-1 (co)receptors and the vast majority of
V24+V11+ 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
V24+V11+ 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 V24+V11+ NKT
cells in determining the rate of progression during HIV-1
infection.
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