The response to TLR ligation of human CD16(+)CD14(-) monocytes is weakly modulated as a consequence of persistent infection with the hepatitis C virus

C Peng, Bisheng Liu, Rob de Knegt, HLA Janssen, Andre Boonstra

Research output: Contribution to journalArticleAcademicpeer-review

7 Citations (Scopus)

Abstract

Little is known about the frequency and function of CD16(+)CD14(-) monocytes from chronic HCV patients. We observed that the absolute numbers and ratio of CD16(+)CD14(-) to CD14(+)CD16(-) monocytes were similar between chronic HCV patients and healthy individuals. Functionally, we found that CD16(+)CD14(-) monocytes are more responsive to TLR8-ligation and only weakly responsive to LPS stimulation in producing TNF as compared to CD14(+)CD16(-) monocytes. We found no overt impairment of the function of CD16(+)CD14(-) monocytes from patients, except for an augmented induction of MIP-1 beta-producing CD16(+)CD14(-) monocytes upon TLR4-ligation. However, the increased frequency of MIP-1 beta-producing CD16(+)CD14(-) monocytes was not associated with viral load, ALT or fibrosis level. Our findings indicate that, different from other infectious diseases, the frequency and function of CD16(+)CD14(-) monocytes are only minimally altered as a consequence of the persistent state of HCV infections, and our findings therefore do not suggest a role for CD16(+)CD14(-) monocytes in HCV pathogenesis. (C) 2011 Elsevier Ltd. All rights reserved.
Original languageUndefined/Unknown
Pages (from-to)1505-1511
Number of pages7
JournalMolecular Immunology
Volume48
Issue number12-13
DOIs
Publication statusPublished - 2011

Research programs

  • EMC MM-04-20-01
  • EMC MM-04-20-02-A

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