Methylation of class II transactivator gene promoter IV is not associated with susceptibility to Multiple Sclerosis

• Main Authors: Lincoln Matthew R (Author), DeLuca Gabriele C (Author), Herrera Blanca M (Author), Morrison Katie M (Author), Dyment David A (Author), Ramagopalan Sreeram V (Author), Orton Sarah M (Author), Handunnetthi Lahiru (Author), Chao Michael J (Author), Sadovnick A Dessa (Author), Ebers George C (Author)
• Format: Book
• Published: BMC, 2008-07-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

<p>Abstract</p> <p>Background</p> <p>Multiple sclerosis (MS) is a complex trait in which alleles at or near the class II loci <it>HLA-DRB1 </it>and <it>HLA-DQB1 </it>contribute significantly to genetic risk. The MHC class II transactivator (<it>MHC2TA</it>) is the master controller of expression of class II genes, and methylation of the promoter of this gene has been previously been shown to alter its function. In this study we sought to assess whether or not methylation of the <it>MHC2TA </it>promoter pIV could contribute to MS disease aetiology.</p> <p>Methods</p> <p>In DNA from peripheral blood mononuclear cells from a sample of 50 monozygotic disease discordant MS twins the <it>MHC2TA </it>promoter IV was sequenced and analysed by methylation specific PCR.</p> <p>Results</p> <p>No methylation or sequence variation of the <it>MHC2TA </it>promoter pIV was found.</p> <p>Conclusion</p> <p>The results of this study cannot support the notion that methylation of the pIV promoter of <it>MHC2TA </it>contributes to MS disease risk, although tissue and timing specific epigenetic modifications cannot be ruled out.</p>

Item Description

10.1186/1471-2350-9-63
1471-2350