Evidence map›Paper›PMID 34108972›Full record

ArticleFrontiers in immunology2021

TLR7 Signaling Drives the Development of Sjögren's Syndrome.

Yawen Wang, Annie Roussel-Queval, Lionel Chasson, Noël Hanna Kazazian, Laetitia Marcadet, Andrianos Nezos, Michael H Sieweke, Clio Mavragani, Lena Alexopoulou

Open access · goldAbstract read
In one paragraph

Article 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 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Advances in Pathogenesis of Sjögren's Syndrome.Journal of immunology research · 2021
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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

9 authors at 4 institutions in 3 countries.

Yawen WangAix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
Annie Roussel-QuevalAix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
Lionel ChassonAix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
Noël Hanna KazazianAix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
Laetitia MarcadetAix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
Andrianos NezosDepartments of Physiology and Pathophysiology, National and Kapodistrian University of Athens School of Medicine, Athens, Greece.
Michael H SiewekeAix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
Clio MavraganiDepartments of Physiology and Pathophysiology, National and Kapodistrian University of Athens School of Medicine, Athens, Greece.
Lena AlexopoulouAix Marseille Univ, CNRS, INSERM, CIML, Marseille, France.
Aix-Marseille Université · FRInserm · FRNational and Kapodistrian University of Athens · GRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sjögren's syndrome (SS) is a chronic systemic autoimmune disease that affects predominately salivary and lacrimal glands. SS can occur alone or in combination with another autoimmune disease like systemic lupus erythematosus (SLE). Here we report that TLR7 signaling drives the development of SS since TLR8-deficient (TLR8ko) mice that develop lupus due to increased TLR7 signaling by dendritic cells, also develop an age-dependent secondary pathology similar to associated SS. The SS phenotype in TLR8ko mice is manifested by sialadenitis, increased anti-SSA and anti-SSB autoantibody production, immune complex deposition and increased cytokine production in salivary glands, as well as lung inflammation. Moreover, ectopic lymphoid structures characterized by B/T aggregates, formation of high endothelial venules and the presence of dendritic cells are formed in the salivary glands of TLR8ko mice. Interestingly, all these phenotypes are abrogated in double TLR7/8-deficient mice, suggesting that the SS phenotype in TLR8-deficient mice is TLR7-dependent. In addition, evaluation of TLR7 and inflammatory markers in the salivary glands of primary SS patients revealed significantly increased

Indexed as

AdultAgedAnimalsChemokinesCytokinesFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedPneumoniaSignal TransductionSjogren's SyndromeToll-Like Receptor 7ChemokinesCytokinesToll-Like Receptor 7autoimmunitydendritic cellsinnate immunitySjögren’s syndrome (SS)TLR7TLR8-deficient micetransgenic mice

Identifiers

PMID34108972
PMCPMC8183380
OpenAlexW3165282158

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.