Sensitization of T cells to CD95-mediated apoptosis by HIV-1 Tat and gp120

THE depletion of CD4+ T cells in AIDS is correlated with high turnover of the human immunodeficiency virus HIV-1,2 and associated with apoptosis3-5. The molecular mechanism of apoptosis in HIV infection, however, is largely unknown. T-cell apoptosis might be affected by viral proteins such as HIV-1...

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Main Authors: Westendorp, Michael (Author) , Frank, Rainer (Author) , Ochsenbauer, Christina (Author) , Stricker, Kirstin (Author) , Dhein, Jens (Author) , Walczak, Henning (Author) , Debatin, Klaus-Michael (Author) , Krammer, Peter H. (Author)
Format: Article (Journal)
Language:English
Published: 08 June 1995
In: Nature
Year: 1995, Volume: 375, Issue: 6531, Pages: 497-500
ISSN:1476-4687
DOI:10.1038/375497a0
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/375497a0
Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/375497a0
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Author Notes:Michael O. Westendorp, Rainer Frank, Christina Ochsenbauer, Kirstin Stricker, Jens Dhein, Henning Walczak, Klaus-Michael Debating, Peter H. Krammer
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Summary:THE depletion of CD4+ T cells in AIDS is correlated with high turnover of the human immunodeficiency virus HIV-1,2 and associated with apoptosis3-5. The molecular mechanism of apoptosis in HIV infection, however, is largely unknown. T-cell apoptosis might be affected by viral proteins such as HIV-1 Tat6-9 and gp120 (refs 10, 11). T-cell-receptor (TCR)-induced apoptosis was recently shown to involve the CD95 (APO-1/Fas) receptor12. We show here that HIV-1 Tat strongly sensitizes TCR- and CD4(gpl20)-induced apoptosis by upregulation of CD95 ligand expression. Concentrations of Tat found to be effective in cultures of HIV-1-infected cells were also observed in sera from HIV-1-infected individuals. Taken together, our results indicate that HIV-1 Tat and gp!20 accelerate CD95-mediated, activation-induced T-cell apoptosis, a mechanism that may contribute to CD4+T-cell depletion5,13,14 in AIDS.
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Physical Description:Online Resource
ISSN:1476-4687
DOI:10.1038/375497a0