Evidence map›Paper›PMID 31092820›Full record

ArticleNature communications2019

Interferon inducible X-linked gene CXorf21 may contribute to sexual dimorphism in Systemic Lupus Erythematosus.

Christopher A Odhams, Amy L Roberts, Susan K Vester, Carolina S T Duarte, Charlie T Beales, Alexander J Clarke, Sonja Lindinger, Samuel J Daffern, Antonino Zito, Lingyan Chen and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
17.3field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. The SLC15A4-TASL complex is essential for lupus development in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
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10 more citing papers are in PubMed but not listed here.

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

17 authors at 4 institutions in 2 countries.

Christopher A OdhamsDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
Amy L RobertsDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
Susan K VesterDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.ORCID http://orcid.org/0000-0002-4210-118X
Carolina S T DuarteDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
Charlie T BealesDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.ORCID http://orcid.org/0000-0003-1297-1448
Alexander J ClarkeKennedy Institute of Rheumatology, University of Oxford, Oxford, OX3 7FY, UK.ORCID http://orcid.org/0000-0003-2846-7860
Sonja LindingerDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
Samuel J DaffernDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.ORCID http://orcid.org/0000-0002-7630-3505
Antonino ZitoDepartment of Twin Research & Genetic Epidemiology, King's College London, London, SE1 7EH, UK.ORCID http://orcid.org/0000-0003-1931-984X
Lingyan ChenDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.ORCID http://orcid.org/0000-0003-3750-6761
Leonardo L JonesDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
Lora BotevaDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
David L MorrisDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.ORCID http://orcid.org/0000-0002-1754-8932
Kerrin S SmallDepartment of Twin Research & Genetic Epidemiology, King's College London, London, SE1 7EH, UK.ORCID http://orcid.org/0000-0003-4566-0005
Michelle M A FernandoDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
Deborah S Cunninghame GrahamDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK.
Timothy J VyseDepartment of Medical & Molecular Genetics, King's College London, London, SE1 9RT, UK. timothy.vyse@kcl.ac.uk.ORCID http://orcid.org/0000-0003-1123-1464
King's College London · GBJohannes Kepler University of Linz · ATQueen Mary University of London · GBUniversity of Oxford · GB

Funding

Arthritis Research UK 20265Arthritis Research UK 20580Medical Research Council MR/M004422/1Medical Research Council MR/R023131/1Versus Arthritis 19983Versus Arthritis 20265Versus Arthritis 20332Versus Arthritis 20580Versus Arthritis 21252Wellcome Trust
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease, characterised by increased expression of type I interferon (IFN)-regulated genes and a striking sex imbalance towards females. Through combined genetic, in silico, in vitro, and ex vivo approaches, we define CXorf21, a gene of hitherto unknown function, which escapes X-chromosome inactivation, as a candidate underlying the Xp21.2 SLE association. We demonstrate that CXorf21 is an IFN-response gene and that the sexual dimorphism in expression is magnified by immunological challenge. Fine-mapping reveals a single haplotype as a potential causal cis-eQTL for CXorf21. We propose that expression is amplified through modification of promoter and 3'-UTR chromatin interactions. Finally, we show that the CXORF21 protein colocalises with TLR7, a pathway implicated in SLE pathogenesis. Our study reveals modulation in gene expression affected by the combination of two hallmarks of SLE: CXorf21 expression increases in a both an IFN-inducible and sex-specific manner.

Indexed as

3' Untranslated RegionsAdultAge FactorsCase-Control StudiesChromosomes, Human, XFemaleGenes, X-LinkedGenetic Predisposition to DiseaseHumansInterferon Type IIntracellular Signaling Peptides and ProteinsLupus Erythematosus, SystemicMalePromoter Regions, GeneticSex FactorsToll-Like Receptor 73' Untranslated RegionsInterferon Type IIntracellular Signaling Peptides and ProteinsTASL protein, humanTLR7 protein, humanToll-Like Receptor 7

Identifiers

PMID31092820
PMCPMC6520347
OpenAlexW2945740253

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.