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• W2131341516 endingPage "3093" @default.
• W2131341516 startingPage "3084" @default.
• W2131341516 abstract "Abstract Cytotoxic T lymphocytes (CTL) lyse antigen-bearing target cells by two distinct pathways. Whereas granule exocytosis targets any antigen-bearing cell, fas-mediated cytotoxicity kills only fas-expressing cells and does not require antigen expression. Fas pathway activation can potentially lead to lysis of uninfected bystander cells. We examined the relative usage of the two pathways by CTL clones and cell lines directed against four different human immunodeficiency virus (HIV) proteins in lysing primary HIV-infected targets. Although fas was expressed on HIV-infected primary CD4+ T cells, their lysis by antigen-specific CD8+ CTL was only by the granule pathway. Fas ligand (fasL) was not detectable on antigen-specific CD8 clones, T-cell lines, or circulating HIV-specific CD8 T cells from HIV-infected donors, stained with a tetrameric HLA-A2-HIV-peptide complex. FasL expression by HIV-specific CTL clones was not activated by exposure to HIV-presenting cells, but was after unphysiological stimulation with phorbol myristate acetate (PMA). CTL clones did not lyse bystander Jurkat cells, but HIV-infected primary CD4+ T cells lysed uninfected bystander cells by the fas-mediated pathway. These results suggest that HIV-specific CD8+ CTL do not cause HIV immunopathology by lysing bystander cells. On the contrary, fas-mediated lysis of uninfected cells by HIV-infected cells may contribute to CD4 decline." @default.
• W2131341516 created "2016-06-24" @default.
• W2131341516 creator A5003060618 @default.
• W2131341516 creator A5031120884 @default.
• W2131341516 creator A5086477957 @default.
• W2131341516 date "1999-11-01" @default.
• W2131341516 modified "2023-09-28" @default.
• W2131341516 title "Viral-Specific Cytotoxic T Lymphocytes Lyse Human Immunodeficiency Virus–Infected Primary T Lymphocytes by the Granule Exocytosis Pathway" @default.
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• W2131341516 doi "https://doi.org/10.1182/blood.v94.9.3084" @default.
• W2131341516 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10556193" @default.
• W2131341516 hasPublicationYear "1999" @default.
• W2131341516 type Work @default.
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• W2131341516 hasAuthorship W2131341516A5086477957 @default.

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