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A polymorphic variant in the MHC2TA gene is not associated with systemic lupus erythematosus
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
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2007 (English)In: Tissue Antigens, ISSN 0001-2815, E-ISSN 1399-0039, Vol. 70, no 5, 412-414 p.Article in journal (Refereed) Published
Abstract [en]

Single-nucleotide polymorphisms (SNPs) in the major histocompatibility complex class II transactivator (MHC2TA) gene encoding the class II transactivator have been associated with multiple sclerosis, rheumatoid arthritis, and myocardial infarction in the Swedish population. We used a case-control approach to investigate the prevalence of a relevant variant in Swedish systemic lupus erythematosus (SLE) cohorts to determine whether SLE shares the same MHC2TA susceptibility allele as the other diseases. No differences were observed between cases and control subjects at either the allele or genotype levels. Furthermore, no significant correlations were found when comparing different clinical and serological SLE phenotypes. This particular polymorphism rs3087456 of the MHC2TA gene does not appear to influence genetic susceptibility to SLE in the Swedish population. We conclude that our data support neither allelic nor genotype association between the MHC2TA SNP and SLE.

Place, publisher, year, edition, pages
2007. Vol. 70, no 5, 412-414 p.
Keyword [en]
Alleles, Case-Control Studies, Female, Genetic Predisposition to Disease, Genotype, Histocompatibility Antigens Class II, Humans, Lupus Erythematosus, Systemic/*genetics, Male, Multiple Sclerosis/genetics, Myocardial Infarction/genetics, Nuclear Proteins/*genetics, Polymorphism, Single Nucleotide, Sweden, Trans-Activators/*genetics
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-13652DOI: 10.1111/j.1399-0039.2007.00920.xISI: 000249994900008PubMedID: 17711409OAI: oai:DiVA.org:uu-13652DiVA: diva2:41422
Available from: 2008-06-02 Created: 2008-06-02 Last updated: 2011-01-26Bibliographically approved

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Publisher's full textPubMedhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=17711409&dopt=Citation

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Nordmark, GunnelRönnblom, Lars
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Department of Genetics and PathologyDepartment of Medical Sciences
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