Evidence map›Paper›PMID 34421926›Full record

ReviewFrontiers in immunology2021

HBV-Specific CD8+ T-Cell Tolerance in the Liver.

Ian Baudi, Keigo Kawashima, Masanori Isogawa

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 69 citations in OpenAlex.

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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.

Ian BaudiDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Keigo KawashimaDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Masanori IsogawaResearch Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Tokyo, Japan.
Nagoya City University · JPNational Institute of Infectious Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) remains a leading cause of liver-related morbidity and mortality through chronic hepatitis that may progress to liver cirrhosis and cancer. The central role played by HBV-specific CD8+ T cells in the clearance of acute HBV infection, and HBV-related liver injury is now well established. Vigorous, multifunctional CD8+ T cell responses are usually induced in most adult-onset HBV infections, while chronic hepatitis B (CHB) is characterized by quantitatively and qualitatively weak HBV-specific CD8+ T cell responses. The molecular basis of this dichotomy is poorly understood. Genomic analysis of dysfunctional HBV-specific CD8+ T cells in CHB patients and various mouse models suggest that multifaceted mechanisms including negative signaling and metabolic abnormalities cooperatively establish CD8+ T cell dysfunction. Immunoregulatory cell populations in the liver, including liver resident dendritic cells (DCs), hepatic stellate cells (HSCs), myeloid-derived suppressor cells (MDSCs), may contribute to intrahepatic CD8+ T cell dysfunction through the production of soluble mediators, such as arginase, indoleamine 2,3-dioxygenase (IDO) and suppressive cytokines and the expression of co-inhibitory molecules. A series of recent studies with mouse models of HBV infection suggest that genetic and epigenetic changes in dysfunctional CD8+ T cells are the manifestation of prolonged antigenic stimulation, as well as the absence of co-stimulatory or cytokine signaling. These new findings may provide potential new targets for immunotherapy aiming at invigorating HBV-specific CD8+ T cells, which hopefully cures CHB.

Indexed as

Immune ToleranceAnimalsAntigensBiomarkersCD8-Positive T-LymphocytesCytotoxicity, ImmunologicEnergy MetabolismEpitopes, T-LymphocyteHepatitis BHepatitis B virusHost-Pathogen InteractionsHumansImmunomodulationLiverLymphocyte ActivationAntigensBiomarkersEpitopes, T-Lymphocyteco-inhibitory signalinghepatitis B virusinterferon signalingintrahepatic antigen recognitionliver tolerancemetabolic regulationT cell exhaustion

Identifiers

PMID34421926
PMCPMC8378532
OpenAlexW3193509611

What OpenQuestion holds

Textmetadata
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.