Evidence map›Paper›PMID 26475932›Full record

ArticleJournal of leukocyte biology2016

HCV-infected cells and differentiation increase monocyte immunoregulatory galectin-9 production.

Noah M K Harwood, Lucy Golden-Mason, Linling Cheng, Hugo R Rosen, John A Mengshol

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed.

  1. Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026
    Review
  2. Review
  3. Galectin-9-An Emerging Glyco-Immune Checkpoint Target for Cancer Therapy.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Galectin-9: diverse roles in skin disease.Frontiers in allergy · 2025
    Review
  6. Review
  7. Extracellular Vesicles inInternational journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Hepatocytes: A key role in liver inflammation.Frontiers in immunology · 2022
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Noah M K HarwoodDivision of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver VA Medical Center, Denver, Colorado, USA.
Lucy Golden-MasonDivision of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver VA Medical Center, Denver, Colorado, USA.
Linling ChengDivision of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver VA Medical Center, Denver, Colorado, USA.
Hugo R RosenDivision of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver VA Medical Center, Denver, Colorado, USA.
John A MengsholDivision of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver VA Medical Center, Denver, Colorado, USA andy.mengshol@ucdenver.edu.

Funding

Hepatitis C viral sensing by non-parenchymal liver cells (NPC)R21AI103361 · NIAID · UNIVERSITY OF COLORADO DENVER · PI ROSEN, HUGO RAMON · 2013 to 2014
$411k
NIAID NIH HHS R21-AI103361
6 · The paper itself

Abstract

The lectin galectin-9 may help establish and maintain chronic hepatitis C virus infection. Galectin-9 is elevated in the liver and sera of hepatitis C virus patients, induces apoptosis of hepatitis C virus-specific T cells, and increases inhibitory regulatory T cells. Kupffer cells stain strongly for galectin-9 protein in hepatitis C virus patients. In the current study, we determined stimuli that induce galectin-9 production by monocytes and macrophages in hepatitis C virus infection. With the use of real-time PCR and flow cytometry, we analyzed galectin-9 mRNA and protein from human monocytes cocultured with hepatitis C virus-infected cells or noninfectious hepatitis C virus subgenomic replicon cells. We focused on finding the stimuli for galectin-9 production. Additionally, we measured galectin-9 during monocyte-to-macrophage maturation. Finally, we examined galectin-9 in peripheral monocytes from hepatitis C virus patients using flow cytometry. Galectin-9 mRNA increased 8-fold when primary monocytes were exposed to hepatitis C virus--infected cells. Maximum induction required proximity or contact and did not require IFN-γ or hepatitis C virus virions. Coculture of monocytes with subgenomic replicon cells increased galectin-9 5-fold, and purified exosomes from infected cells stimulated galectin-9 production. Stimulation of monocyte TLR3, -7, and -8 increased galectin-9 production. Differentiation of monocytes to macrophages increased galectin-9, and nonclassic monocytes from hepatitis C virus patients had the highest levels of galectin-9. Hepatitis C virus-infected cells stimulated monocytes to produce galectin-9 in close proximity, possibly, in part, as a result of exosomes and endosomal TLRs. Differentiation of monocytes to macrophages increased galectin-9. Nonclassic monocytes from hepatitis C virus patients express the highest galectin-9 levels, suggesting they may contribute to elevated galectin-9 and adaptive immune inhibition in hepatitis C virus infection.

Indexed as

Cell CommunicationCell DifferentiationCells, CulturedExosomesGalectinsHepatitis CHepatocytesHumansMacrophagesMonocytesRNA, MessengerToll-Like ReceptorsGalectinsLGALS9 protein, humanRNA, MessengerToll-Like ReceptorsexosomeJFH-1non-classical monocyte

Identifiers

PMID26475932
PMCPMC6608045

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.