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Background/aimsIn most cases infection with hepatitis C results in chronic infection as a consequence of viral subversion and failed anti-viral immune responses. The suggestion that dendritic cells are defective in chronic HCV infection led us to investigate the phenotype and function of liver-derived myeloid (mDC) and plasmacytoid (pDC) dendritic cells in patients with chronic HCV infection.MethodsLiver DCs were isolated without expansion in cytokines from human liver allowing us to study unmanipulated tissue-resident DCs ex vivo.ResultsCompared with mDCs isolated from non-infected inflamed liver mDCs from HCV-infected liver (a) demonstrated higher expression of MHC class II, CD86 and CD123, (b) were more efficient stimulators of allogeneic T-cells and (c) secreted less IL-10. Reduced IL-10 secretion may be a factor in the enhanced functional properties of mDCs from HCV infected liver because antibody depletion of IL-10 enhanced the ability of mDCs from non-infected liver to stimulate T-cells. In contrast, pDCs were present at lower frequencies in HCV-infected liver and expressed higher levels of the regulatory receptor BDCA-2.ConclusionsIn HCV-infected liver the combination of enhanced mDC function and a reduced number of pDCs may contribute to viral persistence in the face of persistent inflammation.

Original publication




Journal article


Journal of hepatology

Publication Date





338 - 347


Liver Research Group, Institute of Biomedical Research, The University of Birmingham Medical School, Wolfson Drive, Edgbaston, Birmingham B15 2TT, UK.


Liver, Plasma Cells, Dendritic Cells, T-Lymphocytes, Granulocyte Precursor Cells, Cells, Cultured, Humans, Hepatitis C, Membrane Glycoproteins, Lectins, C-Type, Receptors, Immunologic, Interleukin-10, Antibodies, Histocompatibility Antigens Class II, Coculture Techniques, Cell Proliferation, Middle Aged, Interleukin-3 Receptor alpha Subunit, B7-2 Antigen