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J Hepatol. 2007 Sep;47(3):338-47. Epub 2007 Apr 12.

Hepatitis C is associated with perturbation of intrahepatic myeloid and plasmacytoid dendritic cell function.

Author information

  • 1Liver Research Group, Institute of Biomedical Research, The University of Birmingham Medical School, Wolfson Drive, Edgbaston, Birmingham B15 2TT, UK. w.k.lai@bham.ac.uk

Abstract

BACKGROUND/AIMS:

In 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.

METHODS:

Liver DCs were isolated without expansion in cytokines from human liver allowing us to study unmanipulated tissue-resident DCs ex vivo.

RESULTS:

Compared 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.

CONCLUSIONS:

In 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.

PMID:
17467113
[PubMed - indexed for MEDLINE]
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