In conclusion, this comprehensive meta-analysis suggested that + 49A/G, - 318C/T, or CT60A/G polymorphism, either in total analysis or in subgroup analyses, has no significant association with MS disease.
Here we show that MS risk modulators converge to alter N-glycosylation and/or CTLA-4 surface retention conditional on metabolism and vitamin D(3), including genetic variants in interleukin-7 receptor-α (IL7RA*C), interleukin-2 receptor-α (IL2RA*T), MGAT1 (IV(A)V(T-T)) and CTLA-4 (Thr17Ala).
There were no significant (P<0.05) associations between the A49G genotype and risk of MS, either before or after stratification for presence of the DR15 haplotype.
Demonstration of prolonged proliferation in patient samples containing the GG genotypes and altered CD152 surface expression was also not demonstrated suggesting that the CD152 exon 1 position 49 A/G dimorphism does not contribute significantly to the development of MS in this patient population.