Journal
TISSUE ANTIGENS
Volume 70, Issue 3, Pages 247-251Publisher
WILEY
DOI: 10.1111/j.1399-0039.2007.00876.x
Keywords
arthritis; genetics; idiopathic; MHC2TA; multiple sclerosis; polymorphism
Categories
Ask authors/readers for more resources
The -168A-G polymorphism has been shown to influence transcription of the MHC2TA gene and has been implicated in several inflammatory/autoimmune disorders. Attempts to reproduce these findings have been inconclusive. We investigated the role of this promoter single nucleotide polymorphism (SNP) in 440 multiple sclerosis (MS), 293 rheumatoid arthritis (RA), 74 juvenile idiopathic arthritis (JIA) patients and 316 healthy controls from Northern Ireland. We also genotyped a non-synonymous SNP in exon 11, +1614G/C. There was no significant difference in the -168G allele frequencies and carriage rates in the separate RA, JIA, or MS collections compared with the control group [odds ratio (OR) = 1.1, 95% confidence intervals (CI) = 0.86-1.44; OR = 1.1, 95% CI = 0.75-1.68; OR = 1.1, 95% CI = 0.84-1.35, respectively]. Assessment of the common phenotype (chronic inflammatory disease; n = 807 vs 316 controls) was negative as well. Carriage of +1614C was protective against JIA (OR = 0.6, 95% CI = 0.3-1.0) and showed a similar trend in RA and MS (OR = 0.7, 95% Cl = 0.5-1.0; OR = 0.8, 95% CI = 0.6-1.0, respectively). The common phenotype (chronic inflaminatory disease) was also significant (OR = 0.7, 95% CI = 0.6-1.0).
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available