Evidence map›Paper›PMID 20932719›Full record

ArticleJournal of autoimmunity2010

CXCL10 promotes liver fibrosis by prevention of NK cell mediated hepatic stellate cell inactivation.

Edith Hintermann, Monika Bayer, Josef M Pfeilschifter, Andrew D Luster, Urs Christen

Abstract read
In one paragraph

Article in Journal of autoimmunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
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

74 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
  2. Article
  3. CXCL10 Regulates Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2026
    Article
  4. Observational
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Protective Effects of Astaxanthin (AST) in the Liver of Weaned Piglets.Animals : an open access journal from MDPI · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Fibrosis-the tale of H3K27 histone methyltransferases and demethylases.Frontiers in cell and developmental biology · 2023
    Review
  20. Article

14 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 2 countries.

Edith HintermannPharmazentrum Frankfurt/ZAFES, Johann Wolfgang Goethe University, Frankfurt am Main, Germany.
Monika Bayer
Josef M Pfeilschifter
Andrew D Luster
Urs Christen
Goethe University Frankfurt · DEMassachusetts General Hospital · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
IP 10--ITS ROLE IN INFLAMMATION AND CANCER THERAPYR01CA069212 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LUSTER, ANDREW D · 1996 to 2014
$5.6M
Development of an animal model for autoimmune hepatitisR21DK071577 · NIDDK · UNIVERSITY OF FRANKFURT · PI CHRISTEN, URS · 2006 to 2007
$158k
NCI NIH HHS R01 CA069212NCI NIH HHS R01-CA069212NIDDK NIH HHS P30 DK043351NIDDK NIH HHS R21 DK071577
6 · The paper itself

Abstract

Chemokines, such as CXCL10, promote hepatic inflammation in chronic or acute liver injury through recruitment of leukocytes to the liver parenchyma. The CXCL10 receptor CXCR3, which is expressed on a subset of leukocytes, plays an important part in Th1-dependent inflammatory responses. Here, we investigated the role of CXCL10 in chemically induced liver fibrosis. We used carbon tetrachloride (CCl(4)) to trigger chronic liver damage in wildtype C57BL/6 and CXCL10-deficient mice. Fibrosis severity was assessed by Sirius Red staining and intrahepatic leukocyte subsets were investigated by immunohistochemistry. We have further analyzed hepatic stellate cell (HSC) distribution and activation and investigated the effect of CXCL10 on HSC motility and proliferation. In order to demonstrate a possible therapeutic intervention strategy, we have examined the anti-fibrotic potential of a neutralizing anti-CXCL10 antibody. Upon CCl(4) administration, CXCL10-deficient mice showed massively reduced liver fibrosis, when compared to wildtype mice. CXCL10-deficient mice had less B- and T lymphocyte and dendritic cell infiltrations within the liver and the number and activity of HSCs was reduced. In contrast, natural killer (NK) cells were more abundant in CXCL10-deficient mice and granzyme B expression was increased in areas with high numbers of NK cells. Further detailed analysis revealed that HSCs express CXCR3, respond to CXCL10 and secrete CXCL10 when stimulated with IFNγ. Blockade of CXCL10 with a neutralizing antibody exhibited a significant anti-fibrotic effect. Our data suggest that CXCL10 is a pro-fibrotic factor, which participates in a crosstalk between hepatocytes, HSCs and immune cells. NK cells seem to play an important role in controlling HSC activity and fibrosis. CXCL10 blockade may constitute a possible therapeutic intervention for hepatic fibrosis.

Indexed as

AnimalsAntibodies, BlockingCarbon TetrachlorideCell MovementCell ProliferationChemokine CXCL10Disease ProgressionGranzymesHepatic Stellate CellsKiller Cells, NaturalLiverLiver CirrhosisMiceMice, Inbred C57BLMice, KnockoutReceptors, CXCR3Antibodies, BlockingCarbon TetrachlorideChemokine CXCL10Cxcr3 protein, mouseGranzymesReceptors, CXCR3

Identifiers

PMID20932719
PMCPMC3855675
OpenAlexW2123002130

What OpenQuestion holds

Textmetadata
LicenceTDM
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.