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Träfflista för sökning "WFRF:(Sollid L M) srt2:(2005-2009)"

Sökning: WFRF:(Sollid L M) > (2005-2009)

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1.
  • Bjornvold, M., et al. (författare)
  • FOXP3 polymorphisms in type 1 diabetes and coeliac disease
  • 2006
  • Ingår i: J Autoimmun. - : Elsevier BV. - 0896-8411. ; 27:2, s. 140-4
  • Tidskriftsartikel (refereegranskat)abstract
    • The FOXP3 gene encodes a transcription factor thought to be essential for the development and function of T regulatory cells. Two previous studies have tested common polymorphisms in FOXP3 for association with type 1 diabetes (T1D) with conflicting results. The aim of our study was to see whether there is any evidence of association between the FOXP3 polymorphisms previously reported to be associated with T1D, in a Caucasian population regarding T1D and coeliac disease (CD). We further looked for evidence of interaction between FOXP3 polymorphisms and HLA-DR3 in conferring susceptibility to T1D. Initially, we analysed two microsatellites in the FOXP3 gene in 363 T1D nuclear families. Our results indicated an association between FOXP3 and T1D (global p=0.004) and a possible interaction between FOXP3 and the HLA-DR3-DQ2 susceptibility haplotype. We then genotyped an additional independent set of 826 T1D patients and 1459 controls as well as one CD dataset consisting of 325 families. A similar tendency was revealed in the CD family material (pnc=0.055 for the associated allele). On the other hand, we were unable to reproduce our initial findings in the T1D case-control dataset (global p=0.6). Our results suggest that the tested FOXP3 markers do not have any major impact on susceptibility for these diseases.
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2.
  • Amundsen, S. S., et al. (författare)
  • Association analysis of MYO9B gene polymorphisms with celiac disease in a Swedish/Norwegian cohort
  • 2006
  • Ingår i: Hum Immunol. - : Elsevier BV. - 0198-8859. ; 67:4-5, s. 341-5
  • Tidskriftsartikel (refereegranskat)abstract
    • Association between myosin IXB (MYO9B) gene variants and celiac disease (CD) has been reported in a study of a Dutch cohort. Six single nucleotide polymorphisms (SNPs) within the 3' part of the MYO9B gene showed significant genetic association and formed an associated haplotype. The current study aimed to replicate these findings in a Swedish/Norwegian cohort. Genotyping of the three SNPs which tagged the associated haplotype was performed in a CD family dataset (n = 326) and in an additional set of healthy controls (n = 562). Although our material provided reasonable power to detect the previously observed association, we were unable to replicate association with these SNPs. Lack of reproducibility could be explained by no or negligible contribution of MYO9B to the genetic predisposition to CD in the Swedish/Norwegian population. Alternatively, it might be due to variable linkage disequilibria in distinct populations in the tested SNPs and a causative mutation yet to be identified or to false positive findings (type I error) in the Dutch study.
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