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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003549naa a2200517 4500
001oai:lup.lub.lu.se:8cf1e0ff-71cd-4555-af26-80e82b2eb83f
003SwePub
008160401s2002 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/3318302 URI
024a https://doi.org/10.1046/j.1469-1809.2002.00102.x2 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Popat, S4 aut
2451 0a Variation in the CTLA4/CD28 gene region confers an increased risk of coeliac disease
264 1b Wiley,c 2002
520 a Susceptibility to coeliae disease involves HLA and non-HLA-linked genes. The CTLA4/CD28 gene region encodes immune regulatory T-cell surface molecules and is a strong candidate as a susceptibility locus. We evaluated CTLA4/CD28 in coeliac disease by genetic linkage and association and combined Our findings with published studies through a meta-analysis. 116 multiplex families were genotyped across CTLA4/CD28 using eight markers. The contribution of CTLA4/CD28 to coeliac disease was assessed by non-parametric linkage and association analyses. Seven studies were identified that had evaluated the relationship between CTLA4/CD28 and coeliac disease and a pooled analysis of data undertaken. In our study there was evidence for a relationship between variation in the CTLA4/CD28 region and coeliae disease by linkage and association analyses. However. the findings did not attain formal statistical significance (p=0.004 and 0.039. respectively). Pooling findings with published results showed significant evidence for linkage (504 families) and association (910 families) : p values. 0.0001 and 0.0014 at D2S2214. respectively. and 0.0008 and 0.0006 at D2S116, respectively. These findings suggest that variation in the CD28/CTLA4 gene region is a determinant of coeliac disease susceptibility. Dissecting the sequence variation underlying this relationship will depend on further analyses utilising denser sets of markers.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng
700a Hearle, N4 aut
700a Hogberg, L4 aut
700a Braegger, CP4 aut
700a O'Donoghue, D4 aut
700a Falth-Magnusson, K4 aut
700a Holmes, GKT4 aut
700a Howdle, PD4 aut
700a Jenkins, H4 aut
700a Johnston, S4 aut
700a Kennedy, NP4 aut
700a Kumar, PJ4 aut
700a Logan, RFA4 aut
700a Marsh, MN4 aut
700a Mulder, CJ4 aut
700a Naluai, AT4 aut
700a Sjöberg, Klasu Lund University,Lunds universitet,Gastroenterologi,Forskargrupper vid Lunds universitet,Enheten för kroniska inflammatoriska och degenerativa sjukdomar,Gastroenterology,Lund University Research Groups,Chronic Inflammatory and Degenerative Diseases Research Unit4 aut0 (Swepub:lu)medf-ksj
700a Stenhammar, L4 aut
700a Walters, JRF4 aut
700a Jewell, DP4 aut
700a Houlston, RS4 aut
710a Gastroenterologib Forskargrupper vid Lunds universitet4 org
773t Annals of Human Geneticsd : Wileyg 66:2, s. 125-137q 66:2<125-137x 1469-1809x 0003-4800
856u http://dx.doi.org/10.1046/j.1469-1809.2002.00102.xy FULLTEXT
8564 8u https://lup.lub.lu.se/record/331830
8564 8u https://doi.org/10.1046/j.1469-1809.2002.00102.x

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