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Fas/FasL-independent activation-induced cell death of T lymphocytes from HIV-infected individuals occurs without DNA fragmentation.

Cellular Immunology

pharmacology, Acetylcysteine, Thiourea, Tetradecanoylphorbol Acetate, ultrastructure, enzymology, drug effects, T-Lymphocytes, classification, T-Lymphocyte Subsets, physiology, Membrane Glycoproteins, Lymphocyte Activation, Ionomycin, Immunophenotyping, Humans, pathology, immunology, HIV Infections, Flow Cytometry, Fas Ligand Protein, DNA Fragmentation, Chromium Radioisotopes, Cells, Cultured, Cell Death, metabolism, Caspases, Antioxidants, Antigens, CD95

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      We assessed the effects of activation with phorbol myrystic acetate (PMA) and ionomycin on peripheral blood mononuclear cells (PBMC) from HIV-infected individuals by (51)Cr release, propidium iodide (PI) uptake, electron microscopy, and DNA analysis. Up to 70% (51)Cr release was induced from PBMC of HIV-infected individuals, versus up to 26% (51)Cr release from PBMC of non-HIV-infected volunteers. Flow cytometry identified mostly T cells undergoing activation-induced cell death (AICD). The kinetics of (51)Cr release and the effects of cold target inhibitors were consistent with cell-mediated cytotoxicity. Certain anti-CD3 antibodies or extracellular Ca(2+) chelation prevented AICD, but antagonistic anti-Fas antibodies, caspase inhibitors, and cycloheximide had no effect. The antioxidants thiourea and N-acetylcysteine reduced AICD, indicating a role for oxidative stress. Electron microscopy revealed plasma membrane disruption with nuclear integrity, while DNA analysis showed intact chromosomal DNA. This form of T cell AICD triggered by PMA and ionomycin differs from classical apoptosis in the absence of either caspase involvement or DNA fragmentation.

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