Genetic Drivers of Epigenetic and Transcriptional Variation in Human Immune Cells

نویسندگان

  • Lu Chen
  • Bing Ge
  • Francesco Paolo Casale
  • Louella Vasquez
  • Tony Kwan
  • Diego Garrido-Martín
  • Stephen Watt
  • Ying Yan
  • Kousik Kundu
  • Simone Ecker
  • Avik Datta
  • David Richardson
  • Frances Burden
  • Daniel Mead
  • Alice L. Mann
  • Jose Maria Fernandez
  • Sophia Rowlston
  • Steven P. Wilder
  • Samantha Farrow
  • Xiaojian Shao
  • John J. Lambourne
  • Adriana Redensek
  • Cornelis A. Albers
  • Vyacheslav Amstislavskiy
  • Sofie Ashford
  • Kim Berentsen
  • Lorenzo Bomba
  • Guillaume Bourque
  • David Bujold
  • Stephan Busche
  • Maxime Caron
  • Shu-Huang Chen
  • Warren Cheung
  • Oliver Delaneau
  • Emmanouil T. Dermitzakis
  • Heather Elding
  • Irina Colgiu
  • Frederik O. Bagger
  • Paul Flicek
  • Ehsan Habibi
  • Valentina Iotchkova
  • Eva Janssen-Megens
  • Bowon Kim
  • Hans Lehrach
  • Ernesto Lowy
  • Amit Mandoli
  • Filomena Matarese
  • Matthew T. Maurano
  • John A. Morris
  • Vera Pancaldi
  • Farzin Pourfarzad
  • Karola Rehnstrom
  • Augusto Rendon
  • Thomas Risch
  • Nilofar Sharifi
  • Marie-Michelle Simon
  • Marc Sultan
  • Alfonso Valencia
  • Klaudia Walter
  • Shuang-Yin Wang
  • Mattia Frontini
  • Stylianos E. Antonarakis
  • Laura Clarke
  • Marie-Laure Yaspo
  • Stephan Beck
  • Roderic Guigo
  • Daniel Rico
  • Joost H.A. Martens
  • Willem H. Ouwehand
  • Taco W. Kuijpers
  • Dirk S. Paul
  • Hendrik G. Stunnenberg
  • Oliver Stegle
  • Kate Downes
  • Tomi Pastinen
  • Nicole Soranzo
چکیده

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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عنوان ژورنال:

دوره 167  شماره 

صفحات  -

تاریخ انتشار 2016