对多发性硬化症患者CD8 + T细胞进行全基因组DNA甲基化分析，结果显示其表观遗传特征与CD4 + T细胞不同。

Genome-wide DNA methylation profiling of CD8+ T cells shows a distinct epigenetic signature to CD4+ T cells in multiple sclerosis patients.

作者信息

Maltby Vicki E, Graves Moira C, Lea Rodney A, Benton Miles C, Sanders Katherine A, Tajouri Lotti, Scott Rodney J, Lechner-Scott Jeannette

机构信息

Centre for Information Based Medicine, Hunter Medical Research Institute, Newcastle, Australia.

School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia.

出版信息

Clin Epigenetics. 2015 Nov 5;7:118. doi: 10.1186/s13148-015-0152-7. eCollection 2015.

DOI:10.1186/s13148-015-0152-7

PMID:26550040

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4635618/

Abstract

BACKGROUND

Multiple sclerosis (MS) is thought to be a T cell-mediated autoimmune disorder. MS pathogenesis is likely due to a genetic predisposition triggered by a variety of environmental factors. Epigenetics, particularly DNA methylation, provide a logical interface for environmental factors to influence the genome. In this study we aim to identify DNA methylation changes associated with MS in CD8+ T cells in 30 relapsing remitting MS patients and 28 healthy blood donors using Illumina 450K methylation arrays.

FINDINGS

Seventy-nine differentially methylated CpGs were associated with MS. The methylation profile of CD8+ T cells was distinctive from our previously published data on CD4+ T cells in the same cohort. Most notably, there was no major CpG effect at the MS risk gene HLA-DRB1 locus in the CD8+ T cells.

CONCLUSION

CD8+ T cells and CD4+ T cells have distinct DNA methylation profiles. This case-control study highlights the importance of distinctive cell subtypes when investigating epigenetic changes in MS and other complex diseases.

摘要

背景

多发性硬化症（MS）被认为是一种由T细胞介导的自身免疫性疾病。MS的发病机制可能是由多种环境因素引发的遗传易感性所致。表观遗传学，尤其是DNA甲基化，为环境因素影响基因组提供了一个合理的切入点。在本研究中，我们旨在使用Illumina 450K甲基化芯片，鉴定30例复发缓解型MS患者和28名健康献血者CD8 + T细胞中与MS相关的DNA甲基化变化。