Evidence map›Paper›PMID 32456348›Full record

ArticleCells2020

Joint Reconstituted Signaling of the IL-6 Receptor via Extracellular Vesicles.

Philipp Arnold, Wiebke Lückstädt, Wenjia Li, Inga Boll, Juliane Lokau, Christoph Garbers, Ralph Lucius, Stefan Rose-John, Christoph Becker-Pauly

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  14. Exploiting the biogenesis of extracellular vesicles for bioengineering and therapeutic cargo loading.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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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 3 institutions in 2 countries.

Philipp ArnoldAnatomical Institute, Christian-Albrechts-University Kiel, Otto-Hahn Platz 8, 24118 Kiel, Germany.ORCID 0000-0003-3273-9865
Wiebke LückstädtAnatomical Institute, Christian-Albrechts-University Kiel, Otto-Hahn Platz 8, 24118 Kiel, Germany.ORCID 0000-0002-1698-6770
Wenjia LiAnatomical Institute, Christian-Albrechts-University Kiel, Otto-Hahn Platz 8, 24118 Kiel, Germany.
Inga BollBiochemical Institute, Christian-Albrechts-University Kiel, Otto-Hahn Platz 9, 24118 Kiel, Germany.
Juliane LokauInstitute of Pathology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany.ORCID 0000-0002-2573-7282
Christoph GarbersInstitute of Pathology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany.
Ralph LuciusAnatomical Institute, Christian-Albrechts-University Kiel, Otto-Hahn Platz 8, 24118 Kiel, Germany.
Stefan Rose-JohnBiochemical Institute, Christian-Albrechts-University Kiel, Otto-Hahn Platz 9, 24118 Kiel, Germany.ORCID 0000-0002-7519-3279
Christoph Becker-PaulyBiochemical Institute, Christian-Albrechts-University Kiel, Otto-Hahn Platz 9, 24118 Kiel, Germany.
Christian-Albrechts-Universität zu Kiel · DEOtto-von-Guericke-Universität Magdeburg · DEUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-6 (IL-6) signaling is a crucial regulatory event important for many biological functions, such as inflammation and tissue regeneration. Accordingly, several pathological conditions are associated with dysregulated IL-6 activity, making it an attractive therapeutic target. For instance, blockade of IL-6 or its α-receptor (IL-6R) by monoclonal antibodies has been successfully used to treat rheumatoid arthritis. However, based on different signaling modes, IL-6 function varies between pro- and anti-inflammatory activity, which is critical for therapeutic intervention. So far, three modes of IL-6 signaling have been described, the classic anti-inflammatory signaling, as well as pro-inflammatory trans-signaling, and trans-presentation. The IL-6/IL-6R complex requires an additional β-receptor (gp130), which is expressed on almost all cells of the human body, to induce STAT3 (signal transducer and activator of signal transcription 3) phosphorylation and subsequent transcriptional regulation. In contrast, the IL-6R is expressed on a limited number of cells, including hepatocytes and immune cells. However, the proteolytic release of the IL-6R enables trans-signaling on cells expressing gp130 only. Here, we demonstrate a fourth possibility of IL-6 signaling that we termed

Indexed as

Signal TransductionCell MembraneCell SurvivalExtracellular VesiclesHEK293 CellsHumansModels, BiologicalPhosphorylationReceptors, Interleukin-6STAT3 Transcription FactorReceptors, Interleukin-6STAT3 protein, humanSTAT3 Transcription Factorchemokineextracellular vesiclesIL-6 receptor signaling

Identifiers

PMID32456348
PMCPMC7291149
OpenAlexW3027473651

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.