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    Additive inhibition of dendritic cell allostimulatory capacity by alcohol and hepatitis C is not restored by DC maturation and involves abnormal IL-10 and IL-2 induction

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    Authors
    Dolganiuc, Angela
    Kodys, Karen
    Kopasz, Andrea
    Marshall, Christopher
    Mandrekar, Pranoti
    Szabo, Gyongyi
    UMass Chan Affiliations
    Department of Medicine, Division of Gastroenterology
    Department of Medicine, Rheumatology Division
    Document Type
    Journal Article
    Publication Date
    2003-06-26
    Keywords
    Adult
    Alcohol Drinking
    Cell Differentiation
    Dendritic Cells
    Ethanol
    Female
    Hepatitis C
    Humans
    Immunosuppression
    Interleukin-10
    Interleukin-2
    Isoantigens
    Male
    Middle Aged
    Myeloid Cells
    Statistics, Nonparametric
    T-Lymphocytes
    Gastroenterology
    Hepatology
    Rheumatology
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    Link to Full Text
    http://dx.doi.org/10.1097/01.ALC.0000071745.63433.32
    Abstract
    BACKGROUND: Excessive alcohol use results in impaired immunity, and it is associated with increased incidence and progression of chronic hepatitis C virus (HCV) infection. Here we investigated the effects of HCV infection and alcohol on myeloid dendritic cells (DC) that are critical in antiviral immunity. METHODS: Immature and mature DCs were generated from monocytes of chronic HCV infected patients (HCV-DC) and controls (N-DC) with IL-4 plus granulocyte-macrophage colony stimulating factor (GM-CSF) in the presence or absence of alcohol (25 mM). DC allostimulatory capacity was tested in mixed lymphocyte reaction (MLR) and cytokine production by ELISA. RESULTS: Allostimulatory capacity of HCV-DCs was reduced compared to N-DCs and it was further inhibited by alcohol treatment (p < 0.01). MLR was also decreased with alcohol-treated N-DCs. DC phenotypic markers and apoptosis were comparable between HCV-DCs and N-DCs irrespective of alcohol treatment. However, HCV-DCs and alcohol-treated N-DCs exhibited elevated IL-10 and reduced IL-12 production. Reduced MLR with HCV-DCs and its further inhibition by alcohol coexisted with decreasing IL-2 levels (p < 0.017). DC maturation partially improved but failed to fully restore the reduced allostimulatory function of either alcohol-treated or alcohol-naive HCV-DCs (p < 0.018). CONCLUSIONS: Alcohol and HCV independently and together inhibit DC allostimulatory capacity, increase IL-10, reduce IL-12 and IL-2 production that cannot be normalized by DC maturation. HCV and alcohol interact to modulate innate and adaptive immune responses via dendritic cells.
    Source
    Alcohol Clin Exp Res. 2003 Jun;27(6):1023-31. Link to article on publisher's site
    DOI
    10.1097/01.ALC.0000071745.63433.32
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/31111
    PubMed ID
    12824825
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1097/01.ALC.0000071745.63433.32
    Scopus Count
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