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Article: Sex-specific association of X-linked toll-like receptor 7 (TLR7) with male systemic lupus erythematosus

TitleSex-specific association of X-linked toll-like receptor 7 (TLR7) with male systemic lupus erythematosus
Authors
Shen, NFu, QDeng, YQian, XZhao, JKaufman, KMWu, YLYu, CYTang, YChen, JYYang, WWong, MKawasaki, ATsuchiya, NSumida, TKawaguchi, YHowe, HSMok, MYBang, SYLiu, FLChang, DMTakasaki, YHashimoto, HHarley, JBGuthridge, JMGrossman, JMCantor, RMSong, YWBae, SCChen, SHahn, BHLau, YLTsao, BP
KeywordsAutoimmunity
Disease susceptibility
Functional polymorphism
Interferon
Type I
Issue Date2010
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2010, v. 107 n. 36, p. 15838-15843 How to Cite?
DOI: http://dx.doi.org/10.1073/pnas.1001337107
AbstractSystemic lupus erythematosus (SLE) is a multisystem, autoimmune disease that predominantly affects women. Previous findings that duplicated Toll-like receptor 7 (Tlr7) promotes lupus-like disease in male BXSB mice prompted us to evaluate TLR7 in human SLE. By using a candidate gene approach, we identified and replicated association of a TLR7 3′UTR SNP, rs3853839 (G/C), with SLE in 9,274 Eastern Asians (P combined = 6.5 × 10 -10), with a stronger effect in male than female subjects [odds ratio, male vs. female = 2.33 (95% CI = 1.64-3.30) vs. 1.24 (95% CI = 1.14-1.34); P = 4.1 × 10 -4]. G-allele carriers had increased TLR7 transcripts and more pronounced IFN signature than C-allele carriers; heterozygotes had 2.7-fold higher transcripts of G-allele than C-allele. These data established a functional polymorphism in type I IFN pathway gene TLR7 predisposing to SLE, especially in Chinese and Japanese male subjects.
Persistent Identifierhttp://hdl.handle.net/10722/139499
ISSN
0027-8424
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
PMC2936646
ISI Accession Number ID
WOS:000281637800040
Funding AgencyGrant Number
Lupus Research Institute
National Institutes of HealthAR043814
AR054459
AR053483
National Natural Science Foundation of China30971632
Shanghai Commission of Science and Technology06JC14050
07ZR14130
08JC1414700
Program of the Shanghai Subject Chief Scientist07XD14021
Ministry for Health, Welfare and Family Affairs, Republic of KoreaA010252
A080588
Japan Society for the Promotion of Science19390271
Ministry of Education, Culture, Sports, Science and Technology of Japan21790935
Veterans Affairs
Funding Information:

We thank all subjects for participation in this study, and H. Wu and Y. Trejo-Lopez for their help in DNA preparation and organization. This work was supported by the Lupus Research Institute, National Institutes of Health Grants AR043814 (to B. P. T.), AR054459 (to C. Y. Y.), and AR053483 (to J.M.G.); National Natural Science Foundation of China Grant 30971632; Program of the Shanghai Commission of Science and Technology Grants 06JC14050, 07ZR14130, and 08JC1414700; Program of the Shanghai Subject Chief Scientist Grant 07XD14021 (to N.S.); Korea Healthcare Technology R&D Project (Ministry for Health, Welfare and Family Affairs, Republic of Korea) Grants A010252 and A080588 (to S. C. B.); Grant-in-Aid for Scientific Research (B; 19390271) from the Japan Society for the Promotion of Science; Grant-in-Aid for Young Scientists (B; 21790935) from the Ministry of Education, Culture, Sports, Science and Technology of Japan (to A. K. and N.T.); and a Veterans Affairs Merit Review Grant (K.M.K.).

References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorShen, Nen_HK
dc.contributor.authorFu, Qen_HK
dc.contributor.authorDeng, Yen_HK
dc.contributor.authorQian, Xen_HK
dc.contributor.authorZhao, Jen_HK
dc.contributor.authorKaufman, KMen_HK
dc.contributor.authorWu, YLen_HK
dc.contributor.authorYu, CYen_HK
dc.contributor.authorTang, Yen_HK
dc.contributor.authorChen, JYen_HK
dc.contributor.authorYang, Wen_HK
dc.contributor.authorWong, Men_HK
dc.contributor.authorKawasaki, Aen_HK
dc.contributor.authorTsuchiya, Nen_HK
dc.contributor.authorSumida, Ten_HK
dc.contributor.authorKawaguchi, Yen_HK
dc.contributor.authorHowe, HSen_HK
dc.contributor.authorMok, MYen_HK
dc.contributor.authorBang, SYen_HK
dc.contributor.authorLiu, FLen_HK
dc.contributor.authorChang, DMen_HK
dc.contributor.authorTakasaki, Yen_HK
dc.contributor.authorHashimoto, Hen_HK
dc.contributor.authorHarley, JBen_HK
dc.contributor.authorGuthridge, JMen_HK
dc.contributor.authorGrossman, JMen_HK
dc.contributor.authorCantor, RMen_HK
dc.contributor.authorSong, YWen_HK
dc.contributor.authorBae, SCen_HK
dc.contributor.authorChen, Sen_HK
dc.contributor.authorHahn, BHen_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorTsao, BPen_HK
dc.date.accessioned2011-09-23T05:50:42Z-
dc.date.available2011-09-23T05:50:42Z-
dc.date.issued2010en_HK
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2010, v. 107 n. 36, p. 15838-15843en_HK
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139499-
dc.description.abstractSystemic lupus erythematosus (SLE) is a multisystem, autoimmune disease that predominantly affects women. Previous findings that duplicated Toll-like receptor 7 (Tlr7) promotes lupus-like disease in male BXSB mice prompted us to evaluate TLR7 in human SLE. By using a candidate gene approach, we identified and replicated association of a TLR7 3′UTR SNP, rs3853839 (G/C), with SLE in 9,274 Eastern Asians (P combined = 6.5 × 10 -10), with a stronger effect in male than female subjects [odds ratio, male vs. female = 2.33 (95% CI = 1.64-3.30) vs. 1.24 (95% CI = 1.14-1.34); P = 4.1 × 10 -4]. G-allele carriers had increased TLR7 transcripts and more pronounced IFN signature than C-allele carriers; heterozygotes had 2.7-fold higher transcripts of G-allele than C-allele. These data established a functional polymorphism in type I IFN pathway gene TLR7 predisposing to SLE, especially in Chinese and Japanese male subjects.en_HK
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_HK
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_HK
dc.subjectAutoimmunityen_HK
dc.subjectDisease susceptibilityen_HK
dc.subjectFunctional polymorphismen_HK
dc.subjectInterferonen_HK
dc.subjectType Ien_HK
dc.subject.meshGenetic Diseases, X-Linked - genetics-
dc.subject.meshGenetic Predisposition to Disease-
dc.subject.meshLupus Erythematosus, Systemic - genetics-
dc.subject.meshSex Factors-
dc.subject.meshToll-Like Receptor 7 - genetics-
dc.titleSex-specific association of X-linked toll-like receptor 7 (TLR7) with male systemic lupus erythematosusen_HK
dc.typeArticleen_HK
dc.identifier.emailYang, W:yangwl@hkucc.hku.hken_HK
dc.identifier.emailMok, MY:temy@hkucc.hku.hken_HK
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_HK
dc.identifier.authorityYang, W=rp00524en_HK
dc.identifier.authorityMok, MY=rp00490en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1001337107en_HK
dc.identifier.pmid20733074-
dc.identifier.pmcidPMC2936646-
dc.identifier.scopuseid_2-s2.0-77957673544en_HK
dc.identifier.hkuros196018en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77957673544&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume107en_HK
dc.identifier.issue36en_HK
dc.identifier.spage15838en_HK
dc.identifier.epage15843en_HK
dc.identifier.isiWOS:000281637800040-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShen, N=7102785475en_HK
dc.identifier.scopusauthoridFu, Q=24067143600en_HK
dc.identifier.scopusauthoridDeng, Y=35104447200en_HK
dc.identifier.scopusauthoridQian, X=36572441800en_HK
dc.identifier.scopusauthoridZhao, J=36572944300en_HK
dc.identifier.scopusauthoridKaufman, KM=7102773191en_HK
dc.identifier.scopusauthoridWu, YL=14219947300en_HK
dc.identifier.scopusauthoridYu, CY=7404977029en_HK
dc.identifier.scopusauthoridTang, Y=13407838200en_HK
dc.identifier.scopusauthoridChen, JY=9043937400en_HK
dc.identifier.scopusauthoridYang, W=23101349500en_HK
dc.identifier.scopusauthoridWong, M=16481455300en_HK
dc.identifier.scopusauthoridKawasaki, A=7102376050en_HK
dc.identifier.scopusauthoridTsuchiya, N=7102607073en_HK
dc.identifier.scopusauthoridSumida, T=7103166990en_HK
dc.identifier.scopusauthoridKawaguchi, Y=7401964647en_HK
dc.identifier.scopusauthoridHowe, HS=7103343933en_HK
dc.identifier.scopusauthoridMok, MY=7006024184en_HK
dc.identifier.scopusauthoridBang, SY=25645654000en_HK
dc.identifier.scopusauthoridLiu, FL=36572216900en_HK
dc.identifier.scopusauthoridChang, DM=7403320055en_HK
dc.identifier.scopusauthoridTakasaki, Y=7101985593en_HK
dc.identifier.scopusauthoridHashimoto, H=36041928300en_HK
dc.identifier.scopusauthoridHarley, JB=7201902945en_HK
dc.identifier.scopusauthoridGuthridge, JM=6602184825en_HK
dc.identifier.scopusauthoridGrossman, JM=7202411114en_HK
dc.identifier.scopusauthoridCantor, RM=35375307600en_HK
dc.identifier.scopusauthoridSong, YW=35075039400en_HK
dc.identifier.scopusauthoridBae, SC=35309443700en_HK
dc.identifier.scopusauthoridChen, S=7410252382en_HK
dc.identifier.scopusauthoridHahn, BH=7201798489en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.scopusauthoridTsao, BP=7005956550en_HK
dc.identifier.issnl0027-8424-

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