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@ARTICLE{Schmiedel:130506,
      author       = {B. J. Schmiedel and G. Seumois and D. Samaniego-Castruita
                      and J. Cayford and V. Schulten and L. Chavez$^*$ and F. Ay
                      and A. Sette and B. Peters and P. Vijayanand},
      title        = {17q21 asthma-risk variants switch {CTCF} binding and
                      regulate {IL}-2 production by {T} cells.},
      journal      = {Nature Communications},
      volume       = {7},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-05585},
      pages        = {13426 -},
      year         = {2016},
      abstract     = {Asthma and autoimmune disease susceptibility has been
                      strongly linked to genetic variants in the 17q21 haploblock
                      that alter the expression of ORMDL3; however, the molecular
                      mechanisms by which these variants perturb gene expression
                      and the cell types in which this effect is most prominent
                      are unclear. We found several 17q21 variants overlapped
                      enhancers present mainly in primary immune cell types.
                      CD4(+) T cells showed the greatest increase (threefold) in
                      ORMDL3 expression in individuals carrying the asthma-risk
                      alleles, where ORMDL3 negatively regulated interleukin-2
                      production. The asthma-risk variants rs4065275 and
                      rs12936231 switched CTCF-binding sites in the 17q21 locus,
                      and 4C-Seq assays showed that several distal cis-regulatory
                      elements upstream of the disrupted ZPBP2 CTCF-binding site
                      interacted with the ORMDL3 promoter region in CD4(+) T cells
                      exclusively from subjects carrying asthma-risk alleles.
                      Overall, our results suggested that T cells are one of the
                      most prominent cell types affected by 17q21 variants.},
      cin          = {B062},
      ddc          = {500},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27848966},
      pmc          = {pmc:PMC5116091},
      doi          = {10.1038/ncomms13426},
      url          = {https://inrepo02.dkfz.de/record/130506},
}