Volume 120, Issue 2 pp. 337-343

HIV-1 matrix protein p17 enhances the proliferative activity of natural killer cells and increases their ability to secrete proinflammatory cytokines

Marco Vitale

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,

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Arnaldo Caruso

Arnaldo Caruso

Chair of Microbiology,

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Maria Antonia De Francesco

Maria Antonia De Francesco

Chair of Microbiology,

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Luigi Rodella

Luigi Rodella

Department of Biomedical Sciences and Biotechnologies, Division of Human Anatomy, and

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Luisa Bozzo

Luisa Bozzo

Chair of Microbiology,

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Emirena Garrafa

Emirena Garrafa

Chair of Microbiology,

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Manuela Grassi

Manuela Grassi

Chair of Microbiology,

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Giuliana Gobbi

Giuliana Gobbi

Division of Clinical Biochemistry, University of Brescia, Brescia, Italy

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Antonio Cacchioli

Antonio Cacchioli

Department of Anatomy, Pharmacology and Forensic Medicine, Ospedale Maggiore, University of Parma, Parma,

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Simona Fiorentini

Simona Fiorentini

Chair of Microbiology,

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First published: 24 January 2003
Citations: 32
Professor Arnaldo Caruso, Chair of Microbiology, University of Brescia Medical School, Piazzale Spedali Civili, 1. 25123 Brescia, Italy. E-mail: [email protected]

Abstract

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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