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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| Hauptverfasser: | , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
08 June 1995
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| In: |
Nature
Year: 1995, Jahrgang: 375, Heft: 6531, Pages: 497-500 |
| ISSN: | 1476-4687 |
| DOI: | 10.1038/375497a0 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/375497a0 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/375497a0 
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| Verfasserangaben: | Michael O. Westendorp, Rainer Frank, Christina Ochsenbauer, Kirstin Stricker, Jens Dhein, Henning Walczak, Klaus-Michael Debating, Peter H. Krammer |
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| 245 | 1 | 0 | |a Sensitization of T cells to CD95-mediated apoptosis by HIV-1 Tat and gp120 |c Michael O. Westendorp, Rainer Frank, Christina Ochsenbauer, Kirstin Stricker, Jens Dhein, Henning Walczak, Klaus-Michael Debating, Peter H. Krammer |
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| 520 | |a 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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