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Activation of natural killer cells by hepatitis C virus particles in vitro.

Abstract

Little is known about the ability of hepatitis C virus (HCV) to alter early innate immune responses in infected patients. Previous studies have shown that natural killer (NK) cells are functionally impaired after interaction of recombinant HCV glycoprotein E2 with the co-stimulatory CD81 molecule in vitro; however, the functional consequences of a prolonged contact of NK cells with HCV particles have remained unclear. We have examined the phenotypes of purified, interleukin-2-activated NK cells from healthy donors and HCV genotype 1b patients after culture for 5 days with HCV pseudoparticles (HCVpp) and serum samples containing HCV genotype 1b. NK cells from healthy donors and chronic HCV patients were found to up-regulate receptors associated with activation (NKp46, NKp44, NKp30, NKG2D), while NK receptors from the killer cell immunoglobulin-like receptor family (KIR/CD158), predominantly having an inhibitory function, were significantly down-modulated after culture in the presence of HCV particles compared with control cultures of NK cells. HCV-infected sera and HCVpp elicited significantly higher secretion of the NK effector lymphokines interferon-γ and tumour necrosis factor-α. Furthermore, HCV stimulated the cytotoxic potential of NK cells from normal donors and patients. The enhanced activation of NK cells after prolonged culture with HCVpp or HCV-containing sera for 5 days suggests that these innate effector cells may play an important role in viral control during early phases of HCV infection.

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  • Authors+Show Affiliations

    ,

    Department of Gastroenterology and Hepatology, Medical Clinic IV, University Hospital of Heidelberg, Heidelberg, Germany.

    , ,

    Source

    Clinical and experimental immunology 165:3 2011 Sep pg 352-62

    MeSH

    Antigens, CD
    Antigens, Differentiation, Myelomonocytic
    CD56 Antigen
    Cell Line, Tumor
    Culture Media, Conditioned
    Cytotoxicity, Immunologic
    GPI-Linked Proteins
    HEK293 Cells
    Hepacivirus
    Humans
    Interferon-gamma
    Killer Cells, Natural
    Lectins
    Lymphocyte Activation
    Lymphocyte Subsets
    NK Cell Lectin-Like Receptor Subfamily D
    NK Cell Lectin-Like Receptor Subfamily K
    Natural Cytotoxicity Triggering Receptor 1
    Natural Cytotoxicity Triggering Receptor 2
    Natural Cytotoxicity Triggering Receptor 3
    Receptors, IgG
    Receptors, KIR
    Tetraspanin 28
    Transfection
    Tumor Necrosis Factor-alpha
    Viral Core Proteins
    Viral Envelope Proteins
    Virion

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    21682720

    Citation

    Farag, M M S., et al. "Activation of Natural Killer Cells By Hepatitis C Virus Particles in Vitro." Clinical and Experimental Immunology, vol. 165, no. 3, 2011, pp. 352-62.
    Farag MM, Weigand K, Encke J, et al. Activation of natural killer cells by hepatitis C virus particles in vitro. Clin Exp Immunol. 2011;165(3):352-62.
    Farag, M. M., Weigand, K., Encke, J., & Momburg, F. (2011). Activation of natural killer cells by hepatitis C virus particles in vitro. Clinical and Experimental Immunology, 165(3), pp. 352-62. doi:10.1111/j.1365-2249.2011.04431.x.
    Farag MM, et al. Activation of Natural Killer Cells By Hepatitis C Virus Particles in Vitro. Clin Exp Immunol. 2011;165(3):352-62. PubMed PMID: 21682720.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Activation of natural killer cells by hepatitis C virus particles in vitro. AU - Farag,M M S, AU - Weigand,K, AU - Encke,J, AU - Momburg,F, Y1 - 2011/06/17/ PY - 2011/6/21/entrez PY - 2011/6/21/pubmed PY - 2011/10/1/medline SP - 352 EP - 62 JF - Clinical and experimental immunology JO - Clin. Exp. Immunol. VL - 165 IS - 3 N2 - Little is known about the ability of hepatitis C virus (HCV) to alter early innate immune responses in infected patients. Previous studies have shown that natural killer (NK) cells are functionally impaired after interaction of recombinant HCV glycoprotein E2 with the co-stimulatory CD81 molecule in vitro; however, the functional consequences of a prolonged contact of NK cells with HCV particles have remained unclear. We have examined the phenotypes of purified, interleukin-2-activated NK cells from healthy donors and HCV genotype 1b patients after culture for 5 days with HCV pseudoparticles (HCVpp) and serum samples containing HCV genotype 1b. NK cells from healthy donors and chronic HCV patients were found to up-regulate receptors associated with activation (NKp46, NKp44, NKp30, NKG2D), while NK receptors from the killer cell immunoglobulin-like receptor family (KIR/CD158), predominantly having an inhibitory function, were significantly down-modulated after culture in the presence of HCV particles compared with control cultures of NK cells. HCV-infected sera and HCVpp elicited significantly higher secretion of the NK effector lymphokines interferon-γ and tumour necrosis factor-α. Furthermore, HCV stimulated the cytotoxic potential of NK cells from normal donors and patients. The enhanced activation of NK cells after prolonged culture with HCVpp or HCV-containing sera for 5 days suggests that these innate effector cells may play an important role in viral control during early phases of HCV infection. SN - 1365-2249 UR - https://www.unboundmedicine.com/medline/citation/21682720/Activation_of_natural_killer_cells_by_hepatitis_C_virus_particles_in_vitro_ L2 - https://doi.org/10.1111/j.1365-2249.2011.04431.x DB - PRIME DP - Unbound Medicine ER -