Evidence map›Paper›PMID 21655107›Full record

ArticlePLoS pathogens2011

Kupffer cells hasten resolution of liver immunopathology in mouse models of viral hepatitis.

Giovanni Sitia, Matteo Iannacone, Roberto Aiolfi, Masanori Isogawa, Nico van Rooijen, Cristina Scozzesi, Marco E Bianchi, Ulrich H von Andrian, Francis V Chisari, Luca G Guidotti

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

67 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
  2. Article
  3. CD4Nature immunology · 2025
    Article
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  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
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  13. Article
  14. Innate immunity and early liver inflammation.Frontiers in immunology · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

7 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

10 authors at 4 institutions in 3 countries.

Giovanni SitiaDivision of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy. sitia.giovanni@hsr.it
Matteo Iannacone
Roberto Aiolfi
Masanori Isogawa
Nico van Rooijen
Cristina Scozzesi
Marco E Bianchi
Ulrich H von Andrian
Francis V Chisari
Luca G Guidotti
Vita-Salute San Raffaele University · ITHarvard University · USScripps Research Institute · USAcademic Medical Center · NL

Funding

PATHOGENESIS OF HEPATITIS B VIRUS IN TRANSGENIC MICER01CA040489 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI CHISARI, FRANCIS VINCENT · 1985 to 2010
$7.7M
PATHOGENESIS OF LIVER DISEASE IN HEPATITISR01AI020001 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI CHISARI, FRANCIS VINCENT · 1985 to 2012
$7.4M
Regulation of HBV Replication by the Immune SystemR01AI040696 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI GUIDOTTI, LUCA G. · 1997 to 2012
$5.2M
Immunological Priming to Hepatitis B VirusR01AI079060 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI ISOGAWA, MASANORI · 2009 to 2012
$1.9M
European Research Council 250219NCI NIH HHS R01 CA040489NCI NIH HHS R01-CA40489NIAID NIH HHS R01 AI020001NIAID NIH HHS R01 AI040696NIAID NIH HHS R01 AI079060NIAID NIH HHS R01-AI079060NIAID NIH HHS R01-AI20001NIAID NIH HHS R01-AI40696
6 · The paper itself

Abstract

Kupffer cells (KCs) are widely considered important contributors to liver injury during viral hepatitis due to their pro-inflammatory activity. Herein we utilized hepatitis B virus (HBV)-replication competent transgenic mice and wild-type mice infected with a hepatotropic adenovirus to demonstrate that KCs do not directly induce hepatocellular injury nor do they affect the pathogenic potential of virus-specific CD8 T cells. Instead, KCs limit the severity of liver immunopathology. Mechanistically, our results are most compatible with the hypothesis that KCs contain liver immunopathology by removing apoptotic hepatocytes in a manner largely dependent on scavenger receptors. Apoptotic hepatocytes not readily removed by KCs become secondarily necrotic and release high-mobility group box 1 (HMGB-1) protein, promoting organ infiltration by inflammatory cells, particularly neutrophils. Overall, these results indicate that KCs resolve rather than worsen liver immunopathology.

Indexed as

AnimalsAnti-Inflammatory AgentsApoptosisBone Density Conservation AgentsCD8-Positive T-LymphocytesClodronic AcidDisease Models, AnimalGadoliniumHepatitis BHepatitis B virusHepatocytesHMGB ProteinsKupffer CellsLiposomesLiverMaleAnti-Inflammatory AgentsBone Density Conservation AgentsClodronic AcidGadoliniumgadolinium chlorideHMGB ProteinsLiposomesReceptors, ScavengerRNA, Messenger

Identifiers

PMID21655107
PMCPMC3107209
OpenAlexW1964879847

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.