Evidence map›Paper›PMID 24913836›Full record

ArticleHepatology (Baltimore, Md.)2014

Immune tolerance in liver disease.

Ian N Crispe

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 2 pooled it
8.7field-weighted citation impact, top 1% 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

154 citing papers in PubMed, 2 syntheses or guidelines pooled it, 263 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. TIGITCancers · 2026
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  8. Review
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  18. The double-positive cells in the tumor microenvironment.Journal of translational internal medicine · 2026
    Article
  19. Neonatal liver niches program T cell tolerance.bioRxiv : the preprint server for biology · 2026
    Article
  20. Review

94 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

1 author at 1 institution in 1 country.

Ian N CrispeDepartment of Pathology, University of Washington Medical Center, Seattle, WA.
University of Washington Medical Center · US

Funding

Kupffer Cells in Liver ImmunopathologyR01AI064463 · NIAID · UNIVERSITY OF ROCHESTER · PI CRISPE, IAN NICHOLAS · 2006 to 2010
$2.0M
T CELL RESPONSES TO LIVER ANTIGENSR01AI063353 · NIAID · UNIVERSITY OF ROCHESTER · PI CRISPE, IAN NICHOLAS · 2005 to 2009
$1.9M
Mouse model of chronic viral hepatitisR01DK075274 · NIDDK · UNIVERSITY OF ROCHESTER · PI CRISPE, IAN NICHOLAS · 2007 to 2011
$1.8M
NIAID NIH HHS R01 AI063353NIAID NIH HHS R01AI064463NIDDK NIH HHS R01 DK075274NIDDK NIH HHS R01DK075274
6 · The paper itself

Abstract

unlabelledLiver tolerance is manifest as a bias toward immune unresponsiveness, both in the context of a major histocompatibility complex-mismatched liver transplant and in the context of liver infection. Two broad classes of mechanisms account for liver tolerance. The presentation of antigens by different liver cell types results in incomplete activation of CD8(+) T cells, usually leading to initial proliferation followed by either clonal exhaustion or premature death of the T cell. Many liver infections result in relatively poor CD4(+) T-cell activation, which may be because liver antigen-presenting cells express a variety of inhibitory cytokines and coinhibitor ligands. Poor CD4(+) T-cell activation by liver antigens likely contributes to abortive activation, exhaustion, and early death of CD8(+) T cells. In addition, a network of active immunosuppressive pathways in the liver is mediated mostly by myeloid cells. Kupffer cells, myeloid-derived suppressor cells, and liver dendritic cells both promote activation of regulatory T cells and suppress CD8(+) and CD4(+) effector T cells. This suppressive network responds to diverse inputs, including signals from hepatocytes, sinusoidal endothelial cells, and hepatic stellate cells.

conclusionThough liver tolerance may be exploited by pathogens, it serves a valuable purpose. Hepatitis A and B infections occasionally elicit a powerful immune response sufficient to cause fatal massive liver necrosis. More commonly, the mechanisms of liver tolerance limit the magnitude of intrahepatic immune responses, allowing the liver to recover. The cost of this adaptive mechanism may be incomplete pathogen eradication, leading to chronic infection.

Indexed as

Immune ToleranceAnimalsDendritic CellsHumansKupffer CellsLiver DiseasesLymphocyte ActivationMyeloid CellsT-Lymphocytes

Identifiers

PMID24913836
PMCPMC4274953
OpenAlexW2137969636

What OpenQuestion holds

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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.