IL-28B Genetic Variants Determine the Extent of Monocyte-Induced Activation of NK Cells in Hepatitis C

PLoS One. 2016 Sep 1;11(9):e0162068. doi: 10.1371/journal.pone.0162068. eCollection 2016.

Abstract

Background: Immuno-genetic studies suggest a functional link between NK cells and λ-IFNs. We recently showed that NK cells are negative for the IFN-λ receptor IFN-λR1 and do not respond to IFN-λ, suggesting a rather indirect association between IL-28B genotype and NK cell activity.

Methods: A total of 75 HCV(+) patients and 67 healthy controls were enrolled into this study. IL-28B (rs12979860) and IFNL-4 (rs368234815) genotypes were determined by rtPCR. Total PBMC, monocytes, and NK cells were stimulated with IL-29, the TLR-7/8 agonist R848, or a combination of both. NK cell IFN-γ response was analysed by FACS. IL-12 and IL-18 secretion of monocytes was studied by ELISA. In blocking experiments anti-IL-12/anti-IL-18 were used.

Results: Following stimulation of total PBMCs with R848 we found NK cell IFN- γ responses to vary with the IL-28B genotype, with carriers of a T/T genotype displaying the lowest frequency of IFN-γ(+)NK cells. When isolated NK cells were studied no such associations were observed, indicating an indirect association between IL-28B genotype and NK cell activity. Accordingly, we found R848-stimulated monocytes of patients with a T/T genotype to be significantly less effective in triggering NK cell IFN- γ production than monocytes from carriers of a non-T/T genotype. In line with these findings we observed monocytes from T/T patients to secrete significantly lower concentrations of IL-12 than monocytes from non-T/T individuals.

Conclusions: Our data indicate that monocytes from carriers of an IL-28B T/T genotype display a reduced ability to stimulate NK cell activity and, thus, provide a link between IL-28B genotype and NK functions.

MeSH terms

  • Female
  • Genetic Variation*
  • Genotype
  • Hepatitis C / genetics*
  • Hepatitis C / immunology*
  • Hepatitis C / metabolism
  • Humans
  • Interferons
  • Interleukin-12 / biosynthesis
  • Interleukins / genetics*
  • Killer Cells, Natural / cytology
  • Killer Cells, Natural / immunology*
  • Lymphocyte Activation / genetics*
  • Male
  • Middle Aged
  • Monocytes / cytology*
  • Monocytes / metabolism

Substances

  • interferon-lambda, human
  • Interleukins
  • Interleukin-12
  • Interferons

Grants and funding

This work was supported by the German Research Foundation (DFG KR 4521/1-1 to BK, and DFG SFB/TR 57 to US and JN) and the H. W. and J. Hector Foundation (M69 to JN). PhD position for BK was funded by DFG KR 4521/1-1. Technician position for CF was funded by DFG SFB/TR 57. Laboratory material was funded by DFG KR 4521/1-1, DFG SFB/TR 57 and the H. W. and J. Hector Foundation. DFG and H. W. and J. Hector Foundation are external funding organizations.The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.