Evidence map›Paper›PMID 32796044›Full record

ArticleAnnals of the rheumatic diseases2020

Contrasting contributions of TNF from distinct cellular sources in arthritis.

Andrey Kruglov, Marina Drutskaya, Dirk Schlienz, Ekaterina Gorshkova, Katharina Kurz, Lars Morawietz, Sergei Nedospasov

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

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  15. Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis.International journal of molecular sciences · 2021
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  20. The many faces of TNF in arthritis.Nature reviews. Rheumatology · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 3 countries.

Andrey KruglovChronic inflammation, Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Berlin, Germany kruglov@drfz.de sergei.nedospasov@gmail.com.ORCID 0000-0002-4597-2087
Marina DrutskayaCenter for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology RAS, Moscow, Russian Federation.
Dirk SchlienzChronic inflammation, Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Berlin, Germany.
Ekaterina GorshkovaCenter for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology RAS, Moscow, Russian Federation.
Katharina KurzChronic inflammation, Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Berlin, Germany.
Lars MorawietzInstitute of Pathology, Medizinischen Versorgungszentrum im Fürstenberg-Karree Berlin, Berlin, Germany.
Sergei NedospasovCenter for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology RAS, Moscow, Russian Federation kruglov@drfz.de sergei.nedospasov@gmail.com.
Engelhardt Institute of Molecular Biology · RUGerman Rheumatism Research Centre · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesNeutralisation of tumour necrosis factor (TNF) is widely used as a therapy for rheumatoid arthritis (RA). However, this therapy is only effective in less than a half of patients and is associated with several side effects. We hypothesised that TNF may possess non-redundant protective and immunomodulatory functions in vivo that cannot be blocked without a cost. The present work aimed to identify cellular sources of protective and pathogenic TNF, and its molecular forms during autoimmune arthritis.

methodsMice lacking TNF expression by distinct cell types, such as myeloid cells and T or B lymphocytes, were subjected to collagen-induced arthritis (CIA) and collagen antibody-induced arthritis. Mice lacking soluble TNF production were also employed. The severity and incidence of the disease, as well as humoral and cellular responses were assessed.

resultsMyeloid cell-derived TNF contributes to both induction and pathogenesis of autoimmune arthritis. Conversely, T cell-derived TNF is protective during the induction phase of arthritis via limiting of interleukin-12 production by dendritic cells and by subsequent control of autoreactive memory T cell development, but is dispensable during the effector phase of arthritis. B cell-derived TNF mediates severity of CIA via control of pathogenic autoantibody production.

conclusionsDistinct TNF-producing cell types may modulate disease development through different mechanisms, suggesting that in arthritis TNF ablation from restricted cellular sources, such as myeloid cells, while preserving protective TNF functions from other cell types may be superior to pan-anti-TNF therapy.

Indexed as

AnimalsArthritis, ExperimentalB-LymphocytesMiceMice, KnockoutMyeloid CellsT-LymphocytesTumor Necrosis Factor-alphaTumor Necrosis Factor-alphaarthritisautoimmunityinflammationT cellstumor necrosis factors

Identifiers

PMID32796044
PMCPMC7569389
OpenAlexW3048516734

What OpenQuestion holds

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LicenceCC BY-NC
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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.