Evidence map›Paper›PMID 29992753›Full record

ArticleJournal of cellular and molecular medicine2018

The involvement of Toll-like receptor 9 in the pathogenesis of erosive autoimmune arthritis.

Anita Fischer, Shahla Abdollahi-Roodsaz, Christina Böhm, Birgit Niederreiter, Brigitte Meyer, Anthony C Y Yau, Erik Lönnblom, Leo A B Joosten, Marije Koenders, Christian H K Lehmann and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

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  2. CpG-A induces liquid-liquid phase separation of HMGB1 to activate the RAGE-mediated inflammatory pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

14 authors at 4 institutions in 5 countries.

Anita FischerDivision of Rheumatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Shahla Abdollahi-RoodsazDepartment of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Christina BöhmDivision of Rheumatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Birgit NiederreiterDivision of Rheumatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Brigitte MeyerDivision of Rheumatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Anthony C Y YauMedical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Erik LönnblomMedical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Leo A B JoostenDepartment of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Marije KoendersDepartment of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Christian H K LehmannDepartment of Dermatology, University Hospital Erlangen, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
Diana DudziakDepartment of Dermatology, University Hospital Erlangen, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
Gerhard KrönkeDepartment of Internal Medicine 3 - Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Rikard HolmdahlMedical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Günter SteinerDivision of Rheumatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-5089-7405
Medical University of Vienna · ATFriedrich-Alexander-Universität Erlangen-Nürnberg · DEKarolinska Institutet · SERadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous nucleic acids and their receptors may be involved in the initiation of systemic autoimmune diseases including rheumatoid arthritis (RA). As the role of the DNA sensing Toll-like receptor (TLR) 9 in RA is unclear, we aimed to investigate its involvement in the pathogenesis of autoimmune arthritis using three different experimental models of RA. The data obtained revealed involvement of TLR9 in the T cell-dependent phase of inflammatory arthritis. In rats with pristane-induced arthritis (PIA), TLR9 inhibition before disease onset reduced arthritis significantly and almost completely abolished bone erosion. Accordingly, serum levels of IL-6, α-1-acid-glycoprotein and rheumatoid factor were reduced. Moreover, in TLR9

Indexed as

AnimalsArthritis, ExperimentalCartilage, ArticularCell WallComplex MixturesGene Expression RegulationInterleukin-6JointsMiceMice, Inbred C57BLMice, KnockoutOrosomucoidOsteoclastsOsteogenesisRatsRheumatoid FactorComplex MixturesIl6 protein, ratInterleukin-6OrosomucoidpristaneRheumatoid FactorTerpenesTLR7 protein, ratTlr9 protein, mouseTlr9 protein, ratToll-Like Receptor 7Toll-Like Receptor 9arthritisbone erosioninflammationosteoclastogenesistoll-like receptor

Identifiers

PMID29992753
PMCPMC6111819
OpenAlexW2811754427

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.