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Publication Detail
Genetic perturbation of PU.1 binding and chromatin looping at neutrophil enhancers associates with autoimmune disease
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Watt S, Vasquez L, Walter K, Mann AL, Kundu K, Chen L, Sims Y, Ecker S, Burden F, Farrow S, Farr B, Iotchkova V, Elding H, Mead D, Tardaguila M, Ponstingl H, Richardson D, Datta A, Flicek P, Clarke L, Downes K, Pastinen T, Fraser P, Frontini M, Javierre B-M, Spivakov M, Soranzo N
  • Publisher:
    Springer Science and Business Media LLC
  • Publication date:
    01/12/2021
  • Journal:
    Nature Communications
  • Volume:
    12
  • Issue:
    1
  • Article number:
    2298
  • Status:
    Published online
  • Language:
    en
Abstract
AbstractNeutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.
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