Evidence map›Paper›PMID 33879788›Full record

ArticleNature communications2021

Loss of α2-6 sialylation promotes the transformation of synovial fibroblasts into a pro-inflammatory phenotype in arthritis.

Yilin Wang, Aneesah Khan, Aristotelis Antonopoulos, Laura Bouché, Christopher D Buckley, Andrew Filer, Karim Raza, Kun-Ping Li, Barbara Tolusso, Elisa Gremese and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-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

35 citing papers in PubMed, 53 citations in OpenAlex.

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  9. St3gal5-mediated sialylation of glyco-CD177 on neutrophils restricts neuroinflammation following CNS injury.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  20. Hyper α2,6-Sialylation Promotes CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
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

15 authors at 7 institutions in 3 countries.

Yilin WangInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Aneesah KhanInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Aristotelis AntonopoulosDepartment of Life Sciences, Imperial College London, London, UK.ORCID http://orcid.org/0000-0002-1592-4092
Laura BouchéDepartment of Life Sciences, Imperial College London, London, UK.
Christopher D BuckleyRheumatology Research Group, Institute for Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Queen Elizabeth Hospital, Birmingham, UK.ORCID http://orcid.org/0000-0001-6924-6402
Andrew FilerRheumatology Research Group, Institute for Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Queen Elizabeth Hospital, Birmingham, UK.ORCID http://orcid.org/0000-0001-8164-6249
Karim RazaRheumatology Research Group, Institute for Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Queen Elizabeth Hospital, Birmingham, UK.
Kun-Ping LiInstitute of Chinese Medicinal Sciences, Guangdong Pharmaceutical University, Guangzhou, China.ORCID http://orcid.org/0000-0003-2364-8988
Barbara TolussoResearch into Inflammatory Arthritis Centre Versus Arthritis (RACE), Glasgow, Birmingham, Newcastle, Oxford, UK.
Elisa GremeseResearch into Inflammatory Arthritis Centre Versus Arthritis (RACE), Glasgow, Birmingham, Newcastle, Oxford, UK.
Mariola Kurowska-StolarskaInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.ORCID http://orcid.org/0000-0003-2124-7777
Stefano AliverniniResearch into Inflammatory Arthritis Centre Versus Arthritis (RACE), Glasgow, Birmingham, Newcastle, Oxford, UK.ORCID http://orcid.org/0000-0002-7383-4212
Anne DellDepartment of Life Sciences, Imperial College London, London, UK.
Stuart M HaslamDepartment of Life Sciences, Imperial College London, London, UK.ORCID http://orcid.org/0000-0002-5563-679X
Miguel A PinedaInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK. miguel.pineda@glasgow.ac.uk.ORCID http://orcid.org/0000-0001-5678-7752
Imperial College London · GBQueen Elizabeth Hospital Birmingham · GBAgostino Gemelli University Polyclinic · ITArthritis UK · GBUniversity of Glasgow · GBGuangdong Pharmaceutical University · CNUniversità Cattolica del Sacro Cuore · IT

Funding

Medical Research Council MR/S025308/1Versus Arthritis 21221Versus Arthritis 22253
6 · The paper itself

Abstract

In healthy joints, synovial fibroblasts (SFs) provide the microenvironment required to mediate homeostasis, but these cells adopt a pathological function in rheumatoid arthritis (RA). Carbohydrates (glycans) on cell surfaces are fundamental regulators of the interactions between stromal and immune cells, but little is known about the role of the SF glycome in joint inflammation. Here we study stromal guided pathophysiology by mapping SFs glycosylation pathways. Combining transcriptomic and glycomic analysis, we show that transformation of fibroblasts into pro-inflammatory cells is associated with glycan remodeling, a process that involves TNF-dependent inhibition of the glycosyltransferase ST6Gal1 and α2-6 sialylation. SF sialylation correlates with distinct functional subsets in murine experimental arthritis and remission stages in human RA. We propose that pro-inflammatory cytokines remodel the SF-glycome, converting the synovium into an under-sialylated and highly pro-inflammatory microenvironment. These results highlight the importance of glycosylation in stromal immunology and joint inflammation.

Indexed as

AnimalsArthritis, ExperimentalArthritis, Rheumatoidbeta-D-Galactoside alpha 2-6-SialyltransferaseCell LineCytokinesDown-RegulationFibroblastsGlycosylationHumansInflammationMaleMetabolic Networks and PathwaysMiceMice, Inbred DBAPhenotypebeta-D-Galactoside alpha 2-6-SialyltransferaseCytokinesSialic AcidsSialyltransferases

Identifiers

PMID33879788
PMCPMC8058094
OpenAlexW3128395018

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.