Evidence map›Paper›PMID 40231469›Full record

ArticleThe Journal of clinical investigation2025

Virus-associated inflammation imprints an inflammatory profile on monocyte-derived macrophages in the human liver.

Juan Diego Sanchez Vasquez, Shirin Nkongolo, Daniel Traum, Valentin Sotov, Samuel C Kim, Deeqa Mahamed, Aman Mehrotra, Anjali Patel, Diana Y Chen, Scott Fung and 7 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026
    Review
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  5. Review
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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

17 authors.

Juan Diego Sanchez VasquezToronto Centre for Liver Disease, Toronto General Hospital Research Institute, and.
Shirin NkongoloDepartment of Internal Medicine IV, University Hospital Heidelberg, Heidelberg, Germany.
Daniel TraumDepartment of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Valentin SotovPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Samuel C KimGilead Sciences, Foster City, California, USA.
Deeqa MahamedCentre for Advanced Single Cell Analysis, The Hospital for Sick Children, Toronto, Canada.
Aman MehrotraToronto Centre for Liver Disease, Toronto General Hospital Research Institute, and.
Anjali PatelSt. Michael's Hospital, Toronto, Canada.
Diana Y ChenGilead Sciences, Foster City, California, USA.
Scott FungToronto Centre for Liver Disease, Toronto General Hospital Research Institute, and.
Anuj GaggarGilead Sciences, Foster City, California, USA.
Jordan J FeldToronto Centre for Liver Disease, Toronto General Hospital Research Institute, and.
Kyong-Mi ChangDepartment of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Jeffrey J WallinGilead Sciences, Foster City, California, USA.
Ben X WangPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Harry LA JanssenDepartment of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, Netherlands.
Adam J GehringToronto Centre for Liver Disease, Toronto General Hospital Research Institute, and.

Funding

Immune regulation and co-stimulation in treatment outcome of chronic hepatitis BU01DK082866 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI CHANG, KYONG-MI · 2008 to 2014
$2.6M
NIDDK NIH HHS U01 DK082866
6 · The paper itself

Abstract

Chronic liver injury triggers the activation and recruitment of immune cells, causing antigen-independent tissue damage and liver disease progression. Tissue inflammation can reshape macrophage composition through monocyte replacement. Replacement of tissue macrophages with monocytes differentiating in an inflammatory environment can potentially imprint a phenotype that switches the liver from an immune-tolerant organ to one predisposed to tissue damage. We longitudinally sampled the liver of patients with chronic hepatitis B who had active liver inflammation and were starting antiviral therapy. Antiviral therapy suppressed viral replication and liver inflammation, which coincided with decreased myeloid activation markers. Single-cell RNA-Seq mapped peripheral inflammatory markers to a monocyte-derived macrophage population, distinct from Kupffer cells, with an inflammatory transcriptional profile. The inflammatory macrophages (iMacs) differentiated from blood monocytes and were unique from macrophage found in healthy or cirrhotic liver. iMacs retained their core transcriptional signature after inflammation resolved, indicating inflammation-mediated remodeling of the macrophage population in the human liver that may affect progressive liver disease and immunotherapy.

Indexed as

Hepatitis B, ChronicHepatitis B virusLiverMacrophagesMonocytesAdultFemaleHumansInflammationKupffer CellsMaleMiddle AgedHepatitisHepatologyImmunologyInfectious diseaseMacrophages

Identifiers

PMID40231469
PMCPMC11996867

What OpenQuestion holds

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LicenceCC BY
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.