期刊
CELL
卷 167, 期 5, 页码 1398-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.10.026
关键词
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资金
- EU FP7 High Impact Project BLUEPRINT [HEALTH-F5-2011-282510]
- Canadian Institutes of Health Research (CIHR) [EP1-120608]
- National Institute for Health Research Cambridge Biomedical Research Centre
- European Molecular Biology Laboratory
- Max Planck Society
- Spanish Ministry of Economy and Competitiveness, Centro de Excelencia Severo Ochoa [SEV-2012-0208]
- Spanish National Bioinformatics Institute (INB-ISCIII) [PT13/0001/0021]
- FEDER Una Manera de hacer Europa
- la Caixa-Severo Ochoa pre-doctoral fellowship
- BHF Cambridge Centre of Excellence [RE/13/6/30180]
- NHS Health Education England
- La Caixa
- FEBS long-term fellowship
- Wellcome Trust [WT098051, WT091310]
- EU FP7 (EPIGENESYS) [257082]
- National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre
- UK Medical Research Council [G0800270]
- British Heart Foundation [SP/09/002]
- UK National Institute for Health Research Cambridge Biomedical Research Centre
- National Institute for Health Research (NIHR)
- Canadian Epigenetics, Environment, and Health Research Consortium (CEEHRC) by the Canadian Institutes of Health Research
- Genome Quebec (CIHR) [EP1-120608]
- Genome Canada
- FRSQ
- Canada Research Chair
- British Heart Foundation [RG/08/014/24067, RG/09/012/28096, RG/13/13/30194] Funding Source: researchfish
- Lundbeck Foundation [R182-2014-3881, R193-2015-1611] Funding Source: researchfish
- Medical Research Council [MR/L003120/1, 1365667, G0800270] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0513-10151, NF-SI-0510-10214, RP-PG-0310-1002, NF-SI-0512-10165] Funding Source: researchfish
- MRC [G0800270, MR/L003120/1] Funding Source: UKRI
Characterizing the multifaceted contribution of genetic and epigenetic factors to disease phenotypes is a major challenge in human genetics and medicine. We carried out high-resolution genetic, epigenetic, and transcriptomic profiling in three major human immune cell types (CD14(+) monocytes, CD16(+) neutrophils, and naive CD4(+) T cells) from up to 197 individuals. We assess, quantitatively, the relative contribution of cis-genetic and epigenetic factors to transcription and evaluate their impact as potential sources of confounding in epigenome-wide association studies. Further, we characterize highly coordinated genetic effects on gene expression, methylation, and histone variation through quantitative trait locus (QTL) mapping and allele-specific (AS) analyses. Finally, we demonstrate colocalization of molecular trait QTLs at 345 unique immune disease loci. This expansive, high-resolution atlas of multi-omics changes yields insights into cell-type-specific correlation between diverse genomic inputs, more generalizable correlations between these inputs, and defines molecular events that may underpin complex disease risk.
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