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10.3389/fimmu.2017.01048 http://scihub22266oqcxt.onion/10.3389/fimmu.2017.01048 C5603903!5603903 !28959253     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28959253 &cmd=llinks): Failed to open stream: HTTP request failed! 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Methylation of the Vitamin D Receptor (VDR) Gene, Together with Genetic Variation, Race, and Environment Influence the Signaling Efficacy of the Toll-Like Receptor 2/1-VDR Pathway |pdf=|usr=}}{{28959253 }} gab.com Text Methylation of the Vitamin D Receptor (VDR) Gene, Together with Genetic Variation, Race, and Environment Influence the Signaling Efficacy of the Toll-Like Receptor 2/1-VDR Pathway JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28959253 #FOAvip BACKGROUND: The disparity in prevalence of infectious diseases across the globe is common knowledge. Vitamin D receptor (VDR)-mediated toll-like receptor (TLR) 2/1 signaling produces antimicrobial peptides, which is critical as a first line of defense in innate immunity. Numerous studies disclosed the independent role of genetic polymorphisms in this pathway, vitamin D status or season and more recently epigenetics, as factors contributing to infectious disease predisposition. Few studies address the interaction between environment, genetics, and epigenetics. Here, we hypothesized that VDR-mediated TLR2/1 signaling is influenced by a combination of environment, epigenetics and genetics, collectively influencing differential innate immunity. METHODS: Healthy Black and White South Africans (n?=?100) donated blood, while ultraviolet index (UVI) was recorded for the duration of the study. LC-MS/MS supported 25(OH)D(3) quantification. Monocyte/macrophage cultures, supplemented with/without 1,25(OH)(2)D(3), were activated with the TLR2/1 elicitor, Pam(3)CSK(4). VDR, cathelicidin antimicrobial peptide, hCAP-18, and 25-hydroxyvitamin D(3)-24-hydroxylase expression were quantified by RT-qPCR or flow cytometry. Pyrosequencing facilitated VDR methylation analysis and single-nucleotide polymorphism (SNP) genotyping in regions pinpointed through a bioinformatics workflow. RESULTS: Season interacted with race showing 25(OH)D(3) deficiency in Blacks. UVI correlated with 25(OH)D(3) and VDR methylation, likely influencing race differences in the latter. Regarding the TLR2/1 pathway, race differences in SNP genotype distribution were confirmed and functional analysis of VDR-mediated signaling showed interaction between race, season, and 25(OH)D(3) status. Multivariate OPLS-DA mirrored several interactions between UVI, 25(OH)D(3) status, DNA sequence, and methylation variants. Methylation of the third cytosine-phosphate-guanine dinucleotide (CpG) in the promoter CpG island (CGI) 1062, CGI 1062 CpG 3, significantly discriminated a 5.7-fold above average mean in VDR protein level upon TLR2/1 elicitation, the variation of which was further influenced by 25(OH)D(3) status and the VDR SNP TaqI. CONCLUSION: Regulation of VDR-mediated TLR2/1 signaling is multifactorial, involving interaction between environment [UVI and consequent 25(OH)D(3) status], epigenetics (VDR methylation at key regulatory sites), and genetics (TLR1, TIRAP, and VDR SNPs). Twit Text FOAVip Methylation of the Vitamin D Receptor (VDR) Gene, Together with Genetic Variation, Race, and Environment Influence the Signaling Efficacy of the Toll-Like Receptor 2/1-VDR Pathway ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28959253 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28959253 #FOAvip English Wikipedia <ref>{{Cite pmid|28959253 }}</ref> Methylation of the Vitamin D Receptor (VDR) Gene, Together with Genetic Variation, Race, and Environment Influence the Signaling Efficacy of the Toll-Like Receptor 2/1-VDR Pathway #MMPMID28959253 Meyer V ; Saccone DS ; Tugizimana F ; Asani FF ; Jeffery TJ ; Bornman L Front Immunol 2017[]; 8 (ä): 1048 PMID28959253 show ga BACKGROUND: The disparity in prevalence of infectious diseases across the globe is common knowledge. Vitamin D receptor (VDR)-mediated toll-like receptor (TLR) 2/1 signaling produces antimicrobial peptides, which is critical as a first line of defense in innate immunity. Numerous studies disclosed the independent role of genetic polymorphisms in this pathway, vitamin D status or season and more recently epigenetics, as factors contributing to infectious disease predisposition. Few studies address the interaction between environment, genetics, and epigenetics. Here, we hypothesized that VDR-mediated TLR2/1 signaling is influenced by a combination of environment, epigenetics and genetics, collectively influencing differential innate immunity. METHODS: Healthy Black and White South Africans (n?=?100) donated blood, while ultraviolet index (UVI) was recorded for the duration of the study. LC-MS/MS supported 25(OH)D(3) quantification. Monocyte/macrophage cultures, supplemented with/without 1,25(OH)(2)D(3), were activated with the TLR2/1 elicitor, Pam(3)CSK(4). VDR, cathelicidin antimicrobial peptide, hCAP-18, and 25-hydroxyvitamin D(3)-24-hydroxylase expression were quantified by RT-qPCR or flow cytometry. Pyrosequencing facilitated VDR methylation analysis and single-nucleotide polymorphism (SNP) genotyping in regions pinpointed through a bioinformatics workflow. RESULTS: Season interacted with race showing 25(OH)D(3) deficiency in Blacks. UVI correlated with 25(OH)D(3) and VDR methylation, likely influencing race differences in the latter. Regarding the TLR2/1 pathway, race differences in SNP genotype distribution were confirmed and functional analysis of VDR-mediated signaling showed interaction between race, season, and 25(OH)D(3) status. Multivariate OPLS-DA mirrored several interactions between UVI, 25(OH)D(3) status, DNA sequence, and methylation variants. Methylation of the third cytosine-phosphate-guanine dinucleotide (CpG) in the promoter CpG island (CGI) 1062, CGI 1062 CpG 3, significantly discriminated a 5.7-fold above average mean in VDR protein level upon TLR2/1 elicitation, the variation of which was further influenced by 25(OH)D(3) status and the VDR SNP TaqI. CONCLUSION: Regulation of VDR-mediated TLR2/1 signaling is multifactorial, involving interaction between environment [UVI and consequent 25(OH)D(3) status], epigenetics (VDR methylation at key regulatory sites), and genetics (TLR1, TIRAP, and VDR SNPs). äMethylation of the Vitamin D Receptor (VDR) Gene, Together with Geneti(epmc).pdf DeepDyve Pubget Overpricing