Evidence map›Paper›PMID 24677194›Full record

ArticleHepatology (Baltimore, Md.)2014

Liver-primed CD8+ T cells suppress antiviral adaptive immunity through galectin-9-independent T-cell immunoglobulin and mucin 3 engagement of high-mobility group box 1 in mice.

Joseph S Dolina, Thomas J Braciale, Young S Hahn

Open access · hybridAbstract 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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

36 citing papers in PubMed, 47 citations in OpenAlex.

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  4. Immune checkpoint TIM-3 in tumor immunotherapy.Acta biochimica et biophysica Sinica · 2026
    Review
  5. TIM-3+ Macrophages: Insights into Their Role in Cancer and Inflammation.International journal of molecular sciences · 2026
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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

3 authors at 2 institutions in 1 country.

Joseph S DolinaDepartment of Microbiology, Immunology, and Cancer Biology, Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, VA.
Thomas J Braciale
Young S Hahn
Carter Center · USUniversity of Virginia · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
INTERDISCIPLINARY TRAINING PROGRAM IN IMMUNOLOGYT32AI007496 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Michael G. Brown, Coleen A McNamara · 1995 to 2026
$10.2M
Regulation of CD8+ T cell responses via liver NK-DC crosstalkU19AI083024 · NIAID · UNIVERSITY OF VIRGINIA · PI HAHN, YOUNG S. · 2009 to 2013
$8.1M
CYTOTOXIC T LYMPHOCYTE RESPONSE TO INFLUENZA VIRUSR01AI015608 · NIAID · WASHINGTON UNIVERSITY · PI BRACIALE, THOMAS J · 1985 to 2017
$5.7M
Role of NK in Regulation of anti-viral T cell immunityR01DK063222 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI HAHN, YOUNG S. · 2003 to 2011
$2.0M
NCI NIH HHS P30 CA044579NIAID NIH HHS R01 AI015608NIAID NIH HHS T32 AI007496NIAID NIH HHS T32 AI07496NIAID NIH HHS U19 AI083024NIDDK NIH HHS DK063222NIDDK NIH HHS R01 DK063222
6 · The paper itself

Abstract

unlabelledThe liver is a tolerogenic environment exploited by persistent infections, such as hepatitis B (HBV) and C (HCV) viruses. In a murine model of intravenous hepatotropic adenovirus infection, liver-primed antiviral CD8(+) T cells fail to produce proinflammatory cytokines and do not display cytolytic activity characteristic of effector CD8(+) T cells generated by infection at an extrahepatic, that is, subcutaneous, site. Importantly, liver-generated CD8(+) T cells also appear to have a T-regulatory (Treg) cell function exemplified by their ability to limit proliferation of antigen-specific T-effector (Teff ) cells in vitro and in vivo via T-cell immunoglobulin and mucin 3 (Tim-3) expressed by the CD8(+) Treg cells. Regulatory activity did not require recognition of the canonical Tim-3 ligand, galectin-9, but was dependent on CD8(+) Treg cell-surface Tim-3 binding to the alarmin, high-mobility group box 1 (HMGB-1).

conclusionVirus-specific Tim-3(+) CD8(+) T cells operating through HMGB-1 recognition in the setting of acute and chronic viral infections of the liver may act to dampen hepatic T-cell responses in the liver microenvironment and, as a consequence, limit immune-mediated tissue injury or promote the establishment of persistent infections.

Indexed as

Adaptive ImmunityAdenoviridaeAdenoviridae InfectionsAnimalsCD8-Positive T-LymphocytesCell ProliferationCellular MicroenvironmentDisease Models, AnimalGalectinsHMGB1 ProteinImmunoglobulinsIn Vitro TechniquesLiverMiceMice, Inbred StrainsMucin-3galectin 9, mouseGalectinsHMGB1 ProteinImmunoglobulinsMucin-3

Identifiers

PMID24677194
PMCPMC3970181
OpenAlexW2072654893

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.