Evidence map›Paper›PMID 30067782›Full record

ArticlePloS one2018

Dysregulation of NF-kB in glandular epithelial cells results in Sjögren's-like features.

Xiaoyan Wang, Abeer Shaalan, Silvia Liefers, Julie Coudenys, Dirk Elewaut, Gordon B Proctor, Hendrika Bootsma, Frans G M Kroese, Sarah Pringle

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  12. Targeted Therapy for Primary Sjögren's Syndrome: Where are We Now?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2021
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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 3 countries.

Xiaoyan WangDepartment of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.
Abeer ShaalanDivision of Mucosal and Salivary Biology, King's College London Dental Institute, King's College London, London, United Kingdom.
Silvia LiefersDepartment of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.
Julie CoudenysDepartment of Rheumatology, Ghent University Hospital, Ghent, Belgium.
Dirk ElewautDepartment of Rheumatology, Ghent University Hospital, Ghent, Belgium.
Gordon B ProctorDivision of Mucosal and Salivary Biology, King's College London Dental Institute, King's College London, London, United Kingdom.
Hendrika BootsmaDepartment of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.
Frans G M KroeseDepartment of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.
Sarah PringleDepartment of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.ORCID 0000-0002-0779-1680
University Medical Center Groningen · NLGhent University Hospital · BEKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The autoimmune disease primary Sjögren's syndrome (pSS) is characterized by hypofunction of the salivary glands (SGs), the cause of which is not correlated to lymphocytic SG infiltration, as prevailing dogma often states. We knocked out the NF-κB proinflammatory pathway inhibitor A20 in keratin14+ epithelial cells, to investigate if immune activated epithelial cells are capable of initiating pSS SG hallmarks. We show that immune activated epithelial cells can cause T cell dominated leukocytic infiltration and immune foci development of the SGs, reflecting the early clinical picture. Infiltrating leukocytes invaded striated ducts, similar to early stage lymphoepithelial lesions observed clinically. Expression of proinflammatory cyto-/chemokines IFNɣ, TNFα, IL-6, CXCL10 and CXCL13 increased in A20-/- SGs, and functionally both volume and mucin 10 content of whole stimulated saliva from A20-/- mice was significantly reduced. Epithelial cells may therefore represent the initial trigger for pSS SG pathologies, as opposed to simple reactionaries to pre-existing stimuli.

Indexed as

AnimalsChemokine CXCL10Chemokine CXCL13Epithelial CellsFemaleInterleukin-6Keratin-14MaleMiceMice, KnockoutMucinsNF-kappa BSalivaSalivary GlandsSjogren's SyndromeT-LymphocytesChemokine CXCL10Chemokine CXCL13Interleukin-6Keratin-14MucinsNF-kappa BTnfaip3 protein, mouseTumor Necrosis Factor-alphaTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID30067782
PMCPMC6070175
OpenAlexW2885149657

What OpenQuestion holds

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LicenceCC BY
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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.