Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases

↓ Direkt till sidans innehåll
↓ Direkt till sidans sekundära innehåll (sidomenyn)

Sökning: WFRF:(Noethen Markus) > Widespread non-addi...

LIBRIS Formathandbok (Information om MARC21)

Fältnamn	Indikatorer	Metadata
000		04381naa a2200769 4500
001		oai:DiVA.org:umu-109376
003		SwePub
008		150925s2015 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:prod.swepub.kib.ki.se:131933968
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1093762 URI
024	7	a https://doi.org/10.1038/ng.33792 DOI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1319339682 URI
040		a (SwePub)umud (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Lenz, Tobias L.4 aut
245	1 0	a Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases
264		c 2015-08-10
264	1	b Macmillan Publishers Ltd.c 2015
338		a print2 rdacarrier
520		a Human leukocyte antigen (HLA) genes confer substantial risk for autoimmune diseases on a log-additive scale. Here we speculated that differences in autoantigen-binding repertoires between a heterozygote's two expressed HLA variants might result in additional non-additive risk effects. We tested the non-additive disease contributions of classical HLA alleles in patients and matched controls for five common autoimmune diseases: rheumatoid arthritis (n(cases) = 5,337), type 1 diabetes (T1D; n(cases) = 5,567), psoriasis vulgaris (n(cases) = 3,089), idiopathic achalasia (n(cases) = 727) and celiac disease (ncases = 11,115). In four of the five diseases, we observed highly significant, non-additive dominance effects (rheumatoid arthritis, P = 2.5 x 10(-12); T1D, P = 2.4 x 10(-10); psoriasis, P = 5.9 x 10(-6); celiac disease, P = 1.2 x 10(-87)). In three of these diseases, the non-additive dominance effects were explained by interactions between specific classical HLA alleles (rheumatoid arthritis, P = 1.8 x 10(-3); T1D, P = 8.6 x 10(-27); celiac disease, P = 6.0 x 10(-100)). These interactions generally increased disease risk and explained moderate but significant fractions of phenotypic variance (rheumatoid arthritis, 1.4%; T1D, 4.0%; celiac disease, 4.1%) beyond a simple additive model.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Hälsovetenskapx Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi0 (SwePub)303022 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Health Sciencesx Public Health, Global Health, Social Medicine and Epidemiology0 (SwePub)303022 hsv//eng
700	1	a Deutsch, Aaron J.4 aut
700	1	a Han, Buhm4 aut
700	1	a Hu, Xinli4 aut
700	1	a Okada, Yukinori4 aut
700	1	a Eyre, Stephen4 aut
700	1	a Knapp, Michael4 aut
700	1	a Zhernakova, Alexandra4 aut
700	1	a Huizinga, Tom W. J.4 aut
700	1	a Abecasis, Goncalo4 aut
700	1	a Becker, Jessica4 aut
700	1	a Boeckxstaens, Guy E.4 aut
700	1	a Chen, Wei-Min4 aut
700	1	a Franke, Andre4 aut
700	1	a Gladman, Dafna D.4 aut
700	1	a Gockel, Ines4 aut
700	1	a Gutierrez-Achury, Javier4 aut
700	1	a Martin, Javier4 aut
700	1	a Nair, Rajan P.4 aut
700	1	a Noethen, Markus M.4 aut
700	1	a Onengut-Gumuscu, Suna4 aut
700	1	a Rahman, Proton4 aut
700	1	a Rantapää-Dahlqvist, Solbritt,d 1947-u Umeå universitet,Reumatologi4 aut0 (Swepub:umu)sora0001
700	1	a Stuart, Philip E.4 aut
700	1	a Tsoi, Lam C.4 aut
700	1	a van Heel, David A.4 aut
700	1	a Worthington, Jane4 aut
700	1	a Wouters, Mira M.4 aut
700	1	a Klareskog, Larsu Karolinska Institutet4 aut
700	1	a Elder, James T.4 aut
700	1	a Gregersen, Peter K.4 aut
700	1	a Schumacher, Johannes4 aut
700	1	a Rich, Stephen S.4 aut
700	1	a Wijmenga, Cisca4 aut
700	1	a Sunyaev, Shamil R.4 aut
700	1	a de Bakker, Paul I. W.4 aut
700	1	a Raychaudhuri, Soumya4 aut
710	2	a Umeå universitetb Reumatologi4 org
773	0	t Nature Geneticsd : Macmillan Publishers Ltd.g 47:9, s. 1085-1090q 47:9<1085-1090x 1061-4036x 1546-1718
856	4	u https://europepmc.org/articles/pmc4552599?pdf=render
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-109376
856	4 8	u https://doi.org/10.1038/ng.3379
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:131933968

Hitta via bibliotek

Nature Genetics (Sök värdpublikationen i LIBRIS)

Till lärosätets databas

Hitta mer i SwePub

Om ämnet

MEDICIN OCH HÄLSOVETENSKAP: MEDICIN OCH HÄLS ...; och Hälsovetenskap; och Folkhälsovetensk ...

Artiklar i publikationen: Nature Genetics

Av lärosätet: Umeå universitet; Karolinska Institutet

Sök utanför SwePub

Sök vidare i:: Google; Google Book Search; Google Scholar

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

LIBRIS.kb.se