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Article: A defunctioning polymorphism in FCGR2B is associated with protection against malaria but susceptibility to systemic lupus erythematosus

TitleA defunctioning polymorphism in FCGR2B is associated with protection against malaria but susceptibility to systemic lupus erythematosus
Authors
KeywordsAutoimmunity
Bacterial septicaemia
Genetic association study
Infectious disease
Selection
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. 17, p. 7881-7885 How to Cite?
AbstractSystemic lupus erythematosus (SLE) is a multisystem autoimmune disease more prevalent in people of African and Asian origin than Caucasian origin. FcγRIIb is an inhibitory Fc receptor with a critical role in immune regulation. Mouse data suggest that FcγRIIb deficiency increases susceptibility to autoimmune disease but protects against infection. We show that a SNP in human FCGR2B that abrogates receptor function is strongly associated with susceptibility to SLE in both Caucasians and Southeast Asians. The minor allele of this SNP is more common in Southeast Asians and Africans, populations from areas where malaria is endemic, than in Caucasians. We show that homozygosity for the minor allele is associated with substantial protection against severe malaria in an East African population (odds ratio = 0.56; P = 7.1 × 10 -5). This protective effect against malaria may contribute to the higher frequency of this SNP and hence, SLE in Africans and Southeast Asians.
Persistent Identifierhttp://hdl.handle.net/10722/125221
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Wellcome Trust083650/Z/07/Z
077092
079895
076934
081835
079082
National Institute for Health Research Cambridge Biomedical Research Centre
BioMalpar Network 6 Network of Excellence
Funding Information:

We thank all patients and controls involved in the study, including the staff and patients at the KEMRI-Wellcome Trust Programme in Kilifi (this paper is published with the permission of the Director of KEMRI). We would also like to thank Kirk A. Rockett, MalariaGEN Research Manager at the Wellcome Trust Centre for Human Genetics, for collation of DNA samples. Financial support was provided by the Wellcome Trust (Programme Grants 083650/Z/07/Z and 077092) and the National Institute for Health Research Cambridge Biomedical Research Centre. The Cambridge Institute for Medical Research is in receipt of Wellcome Trust Strategic Award 079895. This project was also funded by Wellcome Trust Grants 076934 (to T.N.W.), 081835 (to J.A.G.S.), and 079082 (to B.C.U.). T.N.W. and B.C.U. also receive funds from BioMalpar Network 6 Network of Excellence. L.C.W. is a Medical Research Council (MRC) Clinical Training Fellow, K.G.C.S. is a Lister Prize Fellow, and E.J.C. is an MRC Doctoral Training Account student.

References

 

DC FieldValueLanguage
dc.contributor.authorWillcocks, LCen_HK
dc.contributor.authorCarr, EJen_HK
dc.contributor.authorNiederer, HAen_HK
dc.contributor.authorRayner, TFen_HK
dc.contributor.authorWilliams, TNen_HK
dc.contributor.authorYang, Wen_HK
dc.contributor.authorAnthony G Scott, Jen_HK
dc.contributor.authorUrban, BCen_HK
dc.contributor.authorPeshu, Nen_HK
dc.contributor.authorVyse, TJen_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorLyons, PAen_HK
dc.contributor.authorSmith, KGCen_HK
dc.date.accessioned2010-10-31T11:18:21Z-
dc.date.available2010-10-31T11:18:21Z-
dc.date.issued2010en_HK
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2010, v. 107 n. 17, p. 7881-7885en_HK
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125221-
dc.description.abstractSystemic lupus erythematosus (SLE) is a multisystem autoimmune disease more prevalent in people of African and Asian origin than Caucasian origin. FcγRIIb is an inhibitory Fc receptor with a critical role in immune regulation. Mouse data suggest that FcγRIIb deficiency increases susceptibility to autoimmune disease but protects against infection. We show that a SNP in human FCGR2B that abrogates receptor function is strongly associated with susceptibility to SLE in both Caucasians and Southeast Asians. The minor allele of this SNP is more common in Southeast Asians and Africans, populations from areas where malaria is endemic, than in Caucasians. We show that homozygosity for the minor allele is associated with substantial protection against severe malaria in an East African population (odds ratio = 0.56; P = 7.1 × 10 -5). This protective effect against malaria may contribute to the higher frequency of this SNP and hence, SLE in Africans and Southeast Asians.en_HK
dc.languageengen_HK
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.subjectBacterial septicaemiaen_HK
dc.subjectGenetic association studyen_HK
dc.subjectInfectious diseaseen_HK
dc.subjectSelectionen_HK
dc.titleA defunctioning polymorphism in FCGR2B is associated with protection against malaria but susceptibility to systemic lupus erythematosusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0027-8424&volume=107&issue=17&spage=7881&epage=7885&date=2010&atitle=A+defunctioning+polymorphism+in+FCGR2B+is+associated+with+protection+against+malaria+but+susceptibility+to+systemic+lupus+erythematosusen_HK
dc.identifier.emailYang, W:yangwl@hkucc.hku.hken_HK
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_HK
dc.identifier.authorityYang, W=rp00524en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.0915133107en_HK
dc.identifier.pmid20385827-
dc.identifier.pmcidPMC2867866-
dc.identifier.scopuseid_2-s2.0-77951572775en_HK
dc.identifier.hkuros180158en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77951572775&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume107en_HK
dc.identifier.issue17en_HK
dc.identifier.spage7881en_HK
dc.identifier.epage7885en_HK
dc.identifier.isiWOS:000277088700051-
dc.publisher.placeUnited Statesen_HK
dc.identifier.f10003445967-
dc.identifier.scopusauthoridWillcocks, LC=24464597300en_HK
dc.identifier.scopusauthoridCarr, EJ=26425003400en_HK
dc.identifier.scopusauthoridNiederer, HA=24073463900en_HK
dc.identifier.scopusauthoridRayner, TF=12762835400en_HK
dc.identifier.scopusauthoridWilliams, TN=35430527200en_HK
dc.identifier.scopusauthoridYang, W=23101349500en_HK
dc.identifier.scopusauthoridAnthony G Scott, J=36176829400en_HK
dc.identifier.scopusauthoridUrban, BC=7102326026en_HK
dc.identifier.scopusauthoridPeshu, N=7004438094en_HK
dc.identifier.scopusauthoridVyse, TJ=7003955999en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.scopusauthoridLyons, PA=7102522977en_HK
dc.identifier.scopusauthoridSmith, KGC=7410186181en_HK

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