Novel modulating effects of PKC family genes on the relationship between serum vitamin D and relapse in multiple sclerosis

Abstract

Our data support the hypothesis that gene-vitamin D interactions may influence MS clinical course and that the PKC family genes may play a role in the pathogenesis of MS relapse through modulating the association between 25(OH)D and relapse.

Stimulated PBMC-produced IFN- and TNF- are associated with altered relapse risk in multiple sclerosis: results from a prospective cohort study

“…This SNP was directly genotyped in 189 of our samples as part of the ANZgene MS GWAS, extensively described in our previous study 14. Briefly, 164 MS cases were genotyped as a part of ANZgene MS GWAS15 and, additionally, 29 MS case were newly genotyped using the Illumina HumanOmniExpress-12v1_A array.…”

Nutritional factors and aging in demyelinating diseases

“…In a more recent study, involving 141 participants with relapsing-remitting MS, Lin et al studied 276 single nucleotide polymorphisms in 21 genes related to vitamin D metabolism and vitamin D receptor factor complex formation. They hypothesized that the interaction between genes and vitamin D may affect the clinical course of MS and, in particular, that the PKC family genes may be involved in the pathogenesis of relapsing-remitting MS modulating the association between 25(OH)D and relapse (Lin et al 2013).…”

Genetic variation in PBMC-produced IFN-γ and TNF-α associations with relapse in multiple sclerosis

“…This reflects the utility in examining SNPs in parameters relevant to the already demonstrated cytokine risk factors, because by casting the net in this fashion and using a systems biology approach, we have identified results that may uncover modulators of these biological risk factors. Similar approaches have been taken with regard to vitamin D/UV [11][12][13][14], childhood infections [15] and EBV [16] that have either uncovered novel mechanisms of already known risk alleles for MS [12][13][14][15][16] or uncovered novel loci that modulate the course of MS [11].…”

“…A list of these genes and the SNPs are in the Supplemental table. These SNPs were directly genotyped in 189 of our samples as either part of the ANZgene MS GWAS or by an additional GWAS, extensively described in our previous study [5]. Briefly, 164 MS cases were genotyped as a part of ANZgene MS GWAS and additionally 29 MS cases were newly genotyped using the Illumina HumanOmniExpress-12v1_A array.…”