HIV-1 matrix protein p17 enhances the proliferative activity of natural killer cells and increases their ability to secrete proinflammatory cytokines
Marco Vitale
Department of Anatomy, Pharmacology and Forensic Medicine, Ospedale Maggiore, University of Parma, Parma,
Institute of Cytomorphology NP CNR, c/o ‘Codivilla-Putti’ Research Institute, Bologna,
Search for more papers by this authorLuigi Rodella
Department of Biomedical Sciences and Biotechnologies, Division of Human Anatomy, and
Search for more papers by this authorGiuliana Gobbi
Division of Clinical Biochemistry, University of Brescia, Brescia, Italy
Search for more papers by this authorAntonio Cacchioli
Department of Anatomy, Pharmacology and Forensic Medicine, Ospedale Maggiore, University of Parma, Parma,
Search for more papers by this authorMarco Vitale
Department of Anatomy, Pharmacology and Forensic Medicine, Ospedale Maggiore, University of Parma, Parma,
Institute of Cytomorphology NP CNR, c/o ‘Codivilla-Putti’ Research Institute, Bologna,
Search for more papers by this authorLuigi Rodella
Department of Biomedical Sciences and Biotechnologies, Division of Human Anatomy, and
Search for more papers by this authorGiuliana Gobbi
Division of Clinical Biochemistry, University of Brescia, Brescia, Italy
Search for more papers by this authorAntonio Cacchioli
Department of Anatomy, Pharmacology and Forensic Medicine, Ospedale Maggiore, University of Parma, Parma,
Search for more papers by this authorAbstract
Summary. We investigated the effects of human immunodeficiency type-1 virus (HIV-1) matrix protein p17 on freshly isolated and purified human natural killer (NK) cells. HIV-1 p17 increased the cytokines interleukin (IL) 2, IL-12 and IL-15, and induced natural killer cell proliferation, but not cytotoxicity. This effect was specific because it was abrogated by anti-p17 monoclonal antibody. Moreover, HIV-1 p17 enhanced the cytokine-induced production of tumour necrosis factor (TNF)-α and interferon (IFN)-γ by NK cells. IL-4 downregulated IFN-γ and TNF-α secretion in IL-2- and IL-15-treated NK cells. HIV-1 p17 restored the ability of NK cells to produce both cytokines when added to the cultures simultaneously with IL-4. The property of p17 to increase the production of TNF-α and IFN-γ might be a mechanism used by HIV-1 to modulate the immune system to support its replication and spreading.
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