Evidence map›Paper›PMID 34239010›Full record

ArticleScientific reports2021

A myostatin-CCL20-CCR6 axis regulates Th17 cell recruitment to inflamed joints in experimental arthritis.

Michelle Fennen, Toni Weinhage, Vanessa Kracke, Johanna Intemann, Georg Varga, Corinna Wehmeyer, Dirk Foell, Adelheid Korb-Pap, Thomas Pap, Berno Dankbar

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. 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
1.9field-weighted citation impact, top 11% 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, 28 citations in OpenAlex.

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  18. Organokines in Rheumatoid Arthritis: A Critical Review.International journal of molecular sciences · 2022
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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

10 authors at 1 institution in 1 country.

Michelle FennenInstitute of Musculoskeletal Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Bldg. D3, 48149, Muenster, Germany.
Toni WeinhageDepartment of Pediatric Rheumatology and Immunology, University Hospital Muenster, Muenster, Germany.
Vanessa KrackeInstitute of Musculoskeletal Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Bldg. D3, 48149, Muenster, Germany.
Johanna IntemannInstitute of Musculoskeletal Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Bldg. D3, 48149, Muenster, Germany.
Georg VargaDepartment of Pediatric Rheumatology and Immunology, University Hospital Muenster, Muenster, Germany.
Corinna WehmeyerInstitute of Musculoskeletal Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Bldg. D3, 48149, Muenster, Germany.
Dirk FoellDepartment of Pediatric Rheumatology and Immunology, University Hospital Muenster, Muenster, Germany.
Adelheid Korb-PapInstitute of Musculoskeletal Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Bldg. D3, 48149, Muenster, Germany.
Thomas PapInstitute of Musculoskeletal Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Bldg. D3, 48149, Muenster, Germany.
Berno DankbarInstitute of Musculoskeletal Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Bldg. D3, 48149, Muenster, Germany. dankbarb@uni-muenster.de.
University Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interactions of fibroblast-like synoviocyte (FLS)-derived pro-inflammatory cytokines/chemokines and immune cells support the recruitment and activation of inflammatory cells in RA. Here, we show for the first time that the classical myokine myostatin (GDF-8) is involved in the recruitment of Th17 cells to inflammatory sites thereby regulating joint inflammation in a mouse model of TNFalpha-mediated chronic arthritis. Mechanistically, myostatin-deficiency leads to decreased levels of the chemokine CCL20 which is associated with less infiltration of Th17 cells into the inflamed joints. In vitro, myostatin alone or in combination with IL-17A enhances the secretion of CCL20 by FLS whereas myostatin-deficiency reduces CCL20 secretion, associated with an altered transmigration of Th17 cells. Thus, the communication between activated FLS and Th17 cells through myostatin and IL-17A may likely contribute to a vicious cycle of inflammation, accounting for the persistence of joint inflammation in chronic arthritis. Blockade of the CCL20-CCR6 axis by inhibition of myostatin may, therefore, be a promising treatment option for chronic inflammatory diseases such as arthritis.

Indexed as

AnimalsArthritis, RheumatoidCell MovementChemokine CCL20Disease Models, AnimalHumansInflammationInterleukin-17JointsMiceMice, KnockoutMice, TransgenicMyostatinReceptors, CCR6SynoviocytesTh17 CellsCCR6 protein, humanChemokine CCL20Interleukin-17Mstn protein, mouseMyostatinReceptors, CCR6Tumor Necrosis Factor-alpha

Identifiers

PMID34239010
PMCPMC8266846
OpenAlexW3178346488

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Registered trials

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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.