Evidence map›Paper›PMID 22046272›Full record

ArticlePloS one2011

Hepatitis B virus impairs TLR9 expression and function in plasmacytoid dendritic cells.

Isabelle E Vincent, Claudia Zannetti, Julie Lucifora, Helene Norder, Ulrike Protzer, Pierre Hainaut, Fabien Zoulim, Massimo Tommasino, Christian Trépo, Uzma Hasan and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. Pooled it
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  11. Role of extracellular vesicle in human papillomavirus-associated cervical cancer.Journal of cancer research and clinical oncology · 2023
    Review
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  14. Review
  15. Advances in Immunotherapy for Hepatitis B.Pathogens (Basel, Switzerland) · 2022
    Review
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  17. Review
  18. Article
  19. Review
  20. Review

25 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

11 authors at 6 institutions in 3 countries.

Isabelle E VincentINSERM, U871, Lyon, France. isabelle.vincent@inserm.fr
Claudia Zannetti
Julie Lucifora
Helene Norder
Ulrike Protzer
Pierre Hainaut
Fabien Zoulim
Massimo Tommasino
Christian Trépo
Uzma Hasan
Isabelle Chemin
Inserm · FRCentre International de Recherche sur le Cancer · FRHelmholtz Zentrum München · DEHospices Civils de Lyon · FRSwedish Institute · SEUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) play a key role in detecting pathogens by producing large amounts of type I interferon (IFN) by sensing the presence of viral infections through the Toll-Like Receptor (TLR) pathway. TLR9 is a sensor of viral and bacterial DNA motifs and activates the IRF7 transcription factor which leads to type I IFN secretion by pDCs. However, during chronic hepatitis B virus (HBV) infection, pDCs display an impaired ability to secrete IFN-α following ex vivo stimulation with TLR9 ligands. Here we highlight several strategies used by HBV to block IFN-α production through a specific impairment of the TLR9 signaling. Our results show that HBV particle internalisation could inhibit TLR9- but not TLR7-mediated secretion of IFN-α by pDCs. We observed that HBV down-regulated TLR9 transcriptional activity in pDCs and B cells in which TLR9 mRNA and protein levels were reduced. HBV can interfere with TLR9 activity by blocking the MyD88-IRAK4 axis and Sendai virus targeting IRF7 to block IFN-α production. Neutralising CpG motif sequences were identified within HBV DNA genome of genotypes A to H which displayed a suppressive effect on TLR9-immune activation. Moreover, TLR9 mRNA and protein were downregulated in PBMCs from patients with HBV-associated chronic hepatitis and hepatocellular carcinoma. Thus HBV has developed several escape mechanisms to avoid TLR9 activation in both pDCs and B lymphocytes, which may in turn contribute to the establishment and/or persistence of chronic infection.

Indexed as

Immune EvasionB-LymphocytesCarcinoma, HepatocellularCells, CulturedDendritic CellsDown-RegulationHepatitis B, ChronicHepatitis B virusHumansInterferon-alphaLiver NeoplasmsToll-Like Receptor 7Toll-Like Receptor 9Interferon-alphaTLR7 protein, humanTLR9 protein, humanToll-Like Receptor 7Toll-Like Receptor 9

Identifiers

PMID22046272
PMCPMC3201951
OpenAlexW1997332676

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.