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Proximal and distal effects of genetic susceptibility to multiple sclerosis on the T cell epigenome. 2021
Tina Roostaei, and
Hans-Ulrich Klein, and
Yiyi Ma, and
Daniel Felsky, and
Pia Kivisäkk, and
Sarah M Connor, and
Alexandra Kroshilina, and
Christina Yung, and
Belinda J Kaskow, and
Xiaorong Shao, and
Brooke Rhead, and
José M Ordovás, and
Devin M Absher, and
Donna K Arnett, and
Jia Liu, and
Nikolaos Patsopoulos, and
Lisa F Barcellos, and
Howard L Weiner, and
Philip L De Jager
Center for Translational and Computational Neuroimmunology, Department of Neurology and the Taub Institute for Research on Alzheimer's disease and the Aging brain, Columbia University Irving Medical Center, New York, NY, USA.
Identifying the effects of genetic variation on the epigenome in disease-relevant cell types can help advance our understanding of the first molecular contributions of genetic susceptibility to disease onset. Here, we establish a genome-wide map of DNA methylation quantitative trait loci in CD4+ T-cells isolated from multiple sclerosis patients. Utilizing this map in a colocalization analysis, we identify 19 loci where the same haplotype drives both multiple sclerosis susceptibility and local DNA methylation. We also identify two distant methylation effects of multiple sclerosis susceptibility loci: a chromosome 16 locus affects PRDM8 methylation (a chromosome 4 region not previously associated with multiple sclerosis), and the aggregate effect of multiple sclerosis-associated variants in the major histocompatibility complex influences DNA methylation near PRKCA (chromosome 17). Overall, we present a new resource for a key cell type in inflammatory disease research and uncover new gene targets for the study of predisposition to multiple sclerosis.
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