Resolution of a 16.8-Mb autoimmunity-regulating rat chromosome 4 region into multiple encephalomyelitis quantitative trait loci and evidence for epistasis

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Fältnamn	Indikatorer	Metadata
000		03115naa a2200325 4500
001		oai:prod.swepub.kib.ki.se:1946223
003		SwePub
008		240701s2005 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:19462232 URI
024	7	a https://doi.org/10.4049/jimmunol.174.2.9182 DOI
040		a (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Jagodic, Mu Karolinska Institutet4 aut
245	1 0	a Resolution of a 16.8-Mb autoimmunity-regulating rat chromosome 4 region into multiple encephalomyelitis quantitative trait loci and evidence for epistasis
264	1	b The American Association of Immunologists,c 2005
520		a To investigate effects of a 16.8-Mb region on rat chromosome 4q42–43 on encephalomyelitis, we performed a high-resolution mapping using a 10th generation advanced intercross line between the susceptible DA strain and the MHC identical but resistant PVG.1AV1 strain. Clinical signs of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE) developed in 29% of 772 F10 rats. Three regions controlling disease, Eae20, Eae21, and Eae22, were mapped using 15 microsatellite markers spanning 16.8 Mb. Eae20 was a major genetic determinant within the region whereas Eae21 modified disease severity. Eae22 was identified as an epistatic region because it only displayed an effect together with Piebald Virol Glaxo (PVG) alleles on Eae20. Disease down-regulation by PVG alleles in the telomeric part of Eae20 was also demonstrated in DA rats made congenic for a ∼1.44-Mb chromosomal region from PVG. As the region containing Eae20–Eae22 also regulates arthritis, together with the fact that the syntenic mouse 6F2–F3 region regulates experimental lupus and diabetes, and the syntenic human 12p13.31–13.2 region regulates multiple sclerosis and rheumatoid arthritis, the present data point to genes that control several inflammatory diseases. The pairscan analyses of interaction, which here identified Eae22, are novel in the encephalomyelitis field and of importance in the design of further studies of this region in other diseases and species. The limited number of genes identified in Eae20, Eae21, and Eae22 enables focused examination of their relevance in mechanistic animal studies and screening of their association to human diseases.
700	1	a Marta, M4 aut
700	1	a Becanovic, Ku Karolinska Institutet4 aut
700	1	a Sheng, JR4 aut
700	1	a Nohra, R4 aut
700	1	a Olsson, Tu Karolinska Institutet4 aut
700	1	a Lorentzen, JCu Karolinska Institutet4 aut
710	2	a Karolinska Institutet4 org
773	0	t Journal of immunology (Baltimore, Md. : 1950)d : The American Association of Immunologistsg 174:2, s. 918-924q 174:2<918-924x 0022-1767x 1550-6606
856	4	u http://www.jimmunol.org/content/174/2/918.full.pdf
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:1946223
856	4 8	u https://doi.org/10.4049/jimmunol.174.2.918

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Av författaren/redakt...: Jagodic, M; Marta, M; Becanovic, K; Sheng, JR; Nohra, R; Olsson, T; visa fler...; Lorentzen, JC; visa färre...

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Av lärosätet: Karolinska Institutet

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