1. Multiple sclerosis-associated single-nucleotide polymorphisms in CLEC16A correlate with reduced SOCS1 and DEXI expression in the thymus.
- Author
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Leikfoss IS, Mero IL, Dahle MK, Lie BA, Harbo HF, Spurkland A, and Berge T
- Subjects
- Case-Control Studies, Child, DNA-Binding Proteins genetics, Down-Regulation, Genetic Predisposition to Disease, Humans, Membrane Proteins genetics, Suppressor of Cytokine Signaling 1 Protein, Suppressor of Cytokine Signaling Proteins genetics, DNA-Binding Proteins metabolism, Lectins, C-Type genetics, Membrane Proteins metabolism, Monosaccharide Transport Proteins genetics, Multiple Sclerosis genetics, Polymorphism, Single Nucleotide, Suppressor of Cytokine Signaling Proteins metabolism, Thymus Gland metabolism
- Abstract
Genome-wide association studies have revealed that the 16p13 chromosomal region, including CLEC16A, DEXI, CIITA and SOCS1, is associated with susceptibility to autoimmune diseases. As non-coding single-nucleotide polymorphisms (SNPs) may confer susceptibility to disease by affecting expression of nearby genes, we examined whether autoimmune-associated intronic CLEC16A SNPs (rs12708716, rs6498169 and rs7206912) correlate with the expression of CLEC16A itself as well as neighboring genes in whole-blood and thymic samples. Real-time quantitative PCR analyses show that SOCS1 and DEXI expression was lower in thymic samples carrying at least one of the CLEC16A risk alleles compared with non-carriers of the risk allele. Linear regression analysis revealed a significant correlation between the expression level of CLEC16A and that of SOCS1 and DEXI in thymic samples. These data indicate a possible regulatory role for multiple sclerosis-associated non-coding CLEC16A SNPs and a common control mechanism for the expression of CLEC16A, SOCS1 and DEXI.
- Published
- 2013
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