1. HIV-1 matrix protein p17 enhances the proliferative activity of natural killer cells and increases their ability to secrete proinflammatory cytokines.
- Author
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Vitale M, Caruso A, De Francesco MA, Rodella L, Bozzo L, Garrafa E, Grassi M, Gobbi G, Cacchioli A, and Fiorentini S
- Subjects
- Antibodies, Monoclonal pharmacology, Cell Division drug effects, Cells, Cultured, Gene Products, gag immunology, HIV Antigens immunology, Humans, Interferon-gamma biosynthesis, Interleukin-12 metabolism, Interleukin-12 pharmacology, Interleukin-15 metabolism, Interleukin-15 pharmacology, Interleukin-2 metabolism, Interleukin-2 pharmacology, Interleukin-4 pharmacology, Killer Cells, Natural drug effects, Killer Cells, Natural immunology, Recombinant Proteins pharmacology, Stimulation, Chemical, Tumor Necrosis Factor-alpha biosynthesis, gag Gene Products, Human Immunodeficiency Virus, Cytokines metabolism, Gene Products, gag pharmacology, HIV Antigens pharmacology, Killer Cells, Natural metabolism, Viral Proteins
- Abstract
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)-alpha and interferon (IFN)-gamma by NK cells. IL-4 downregulated IFN-gamma and TNF-alpha 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-alpha and IFN-gamma might be a mechanism used by HIV-1 to modulate the immune system to support its replication and spreading.
- Published
- 2003
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