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Erschienen in:
01.09.2008
IkBα Promoter Polymorphisms in Patients with Primary Sjögren’s Syndrome
Erschienen in: Journal of Clinical Immunology | Ausgabe 5/2008
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Introduction
To investigate the association of IkBα promoter polymorphisms with the development of primary Sjögren’s syndrome in Taiwan, 98 patients with primary Sjögren’s syndrome and 110 unrelated healthy controls were enrolled in this study.
Materials and Methods
The IκBα −881 A/G, IκBα −826 C/T, IκBα −550 A/T, IκBα −519 C/T, and IκBα −297 C/T polymorphisms were determined by the methods of polymerase chain reaction/restriction fragment length polymorphism.
Results
This study demonstrated that the genotype frequencies of IκBα −826 C/T and IκBα −826 T/T, in comparison with that of IκBα −826 C/C, were significantly higher in the patients with primary Sjögren’s syndrome than in the controls. The allele frequency of IκBα −881 G was significantly decreased in the patients with primary Sjögren’s syndrome compared with that of the controls. In contrast, the allele frequency of IκBα −826 T was significantly higher in the patients with primary Sjögren’s syndrome than in the controls. The similar findings could also be found in the allele carriage frequencies. The patients with primary Sjögren’s syndrome had lower allele carriage frequencies of IκBα −881 G and IκBα −826 C, and a higher allele carriage frequency of IκBα −826 T. We also found that the estimated haplotype frequency of IκBα −881A-826T-550A-519C-297C was significantly increased in the patients with primary Sjögren’s syndrome in comparison with that of the controls.
Discussion
This study demonstrated that the IkBα −826T allele and IkBα −881A-826T-550A-519C-297C haplotype were associated with susceptibility to primary Sjögren’s syndrome in Taiwan. However, these findings may not be disease-specific but may be related to inflammatory responses.