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Article: Independent Replication on Genome-Wide Association Study Signals Identifies IRF3 as a Novel Locus for Systemic Lupus Erythematosus

TitleIndependent Replication on Genome-Wide Association Study Signals Identifies IRF3 as a Novel Locus for Systemic Lupus Erythematosus
Authors
Keywordsgenome-wide association study
replication
IRF3
systemic lupus erythematosus
lupus nephritis
Issue Date2020
PublisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/genetics
Citation
Frontiers in Genetics, 2020, v. 11, p. article no. 600 How to Cite?
AbstractSystemic lupus erythematosus (SLE) is a genetically complex autoimmune disease. Despite the significant progress made in identifying susceptibility genes for SLE, the genetic architecture of the disease is far from being understood. In this study, we set to replicate a number of suggestive association signals found in genome-wide association studies (GWASs) in additional independent cohorts. Replication studies were performed on Han Chinese cohorts from Hong Kong and Anhui, involving a total of 2,269 cases and 5,073 controls. We identified a missense variant in IRF3 (rs7251) reaching genome-wide significance through a joint analysis of GWAS and replication data (OR = 0.876, P = 4.40E-08). A significant correlation was observed between rs7251 and lupus nephritis (LN) by subphenotype stratification (OR = 0.785, P = 0.0128). IRF3 is a key molecule in type I interferon production upon nucleic acid antigen stimulations and may inhibit regulatory T cell differentiation. Further elucidation of the mechanism of this association could help us better understand the pathogenesis of SLE.
Persistent Identifierhttp://hdl.handle.net/10722/285480
ISSN
2023 Impact Factor: 2.8
2023 SCImago Journal Rankings: 0.853
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, F-
dc.contributor.authorWang, YF-
dc.contributor.authorZhang, Y-
dc.contributor.authorLin, Z-
dc.contributor.authorCAO, Y-
dc.contributor.authorZHANG, H-
dc.contributor.authorLIU, ZY-
dc.contributor.authorMorris, DL-
dc.contributor.authorSheng, Y-
dc.contributor.authorCui, Y-
dc.contributor.authorZhang, X-
dc.contributor.authorVyse, TJ-
dc.contributor.authorLau, YL-
dc.contributor.authorYang, W-
dc.contributor.authorChen, Y-
dc.date.accessioned2020-08-18T03:53:49Z-
dc.date.available2020-08-18T03:53:49Z-
dc.date.issued2020-
dc.identifier.citationFrontiers in Genetics, 2020, v. 11, p. article no. 600-
dc.identifier.issn1664-8021-
dc.identifier.urihttp://hdl.handle.net/10722/285480-
dc.description.abstractSystemic lupus erythematosus (SLE) is a genetically complex autoimmune disease. Despite the significant progress made in identifying susceptibility genes for SLE, the genetic architecture of the disease is far from being understood. In this study, we set to replicate a number of suggestive association signals found in genome-wide association studies (GWASs) in additional independent cohorts. Replication studies were performed on Han Chinese cohorts from Hong Kong and Anhui, involving a total of 2,269 cases and 5,073 controls. We identified a missense variant in IRF3 (rs7251) reaching genome-wide significance through a joint analysis of GWAS and replication data (OR = 0.876, P = 4.40E-08). A significant correlation was observed between rs7251 and lupus nephritis (LN) by subphenotype stratification (OR = 0.785, P = 0.0128). IRF3 is a key molecule in type I interferon production upon nucleic acid antigen stimulations and may inhibit regulatory T cell differentiation. Further elucidation of the mechanism of this association could help us better understand the pathogenesis of SLE.-
dc.languageeng-
dc.publisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/genetics-
dc.relation.ispartofFrontiers in Genetics-
dc.rightsThis Document is Protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectgenome-wide association study-
dc.subjectreplication-
dc.subjectIRF3-
dc.subjectsystemic lupus erythematosus-
dc.subjectlupus nephritis-
dc.titleIndependent Replication on Genome-Wide Association Study Signals Identifies IRF3 as a Novel Locus for Systemic Lupus Erythematosus-
dc.typeArticle-
dc.identifier.emailWang, YF: yfwangbm@connect.hku.hk-
dc.identifier.emailLau, YL: lauylung@hku.hk-
dc.identifier.emailYang, W: yangwl@hku.hk-
dc.identifier.authorityLau, YL=rp00361-
dc.identifier.authorityYang, W=rp00524-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3389/fgene.2020.00600-
dc.identifier.pmid32719713-
dc.identifier.pmcidPMC7348047-
dc.identifier.scopuseid_2-s2.0-85088459123-
dc.identifier.hkuros312932-
dc.identifier.volume11-
dc.identifier.spagearticle no. 600-
dc.identifier.epagearticle no. 600-
dc.identifier.isiWOS:000553963500001-
dc.publisher.placeSwitzerland-
dc.identifier.issnl1664-8021-

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