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@ARTICLE{Stanifer:148628,
      author       = {M. Stanifer$^*$ and M. Mukenhirn$^*$ and S. Muenchau$^*$
                      and K. Pervolaraki$^*$ and T. Kanaya and D. Albrecht$^*$ and
                      C. Odendall and T. Hielscher$^*$ and V. Haucke and J. C.
                      Kagan and S. Bartfeld and H. Ohno and S. Boulant$^*$},
      title        = {{A}symmetric distribution of {TLR}3 leads to a polarized
                      immune response in human intestinal epithelial cells.},
      journal      = {Nature microbiology},
      volume       = {5},
      number       = {1},
      issn         = {2058-5276},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2019-03173},
      pages        = {181-191},
      year         = {2020},
      note         = {2020 Jan;5(1):181-191#EA:F140#LA:F140#},
      abstract     = {Intestinal epithelial cells (IECs) act as a physical
                      barrier separating the commensal-containing intestinal tract
                      from the sterile interior. These cells have found a complex
                      balance allowing them to be prepared for pathogen attacks
                      while still tolerating the presence of bacterial or viral
                      stimuli present in the lumen of the gut. Using primary human
                      IECs, we probed the mechanisms that allow for such a
                      tolerance. We discovered that viral infections emanating
                      from the basolateral side of IECs elicit a stronger
                      intrinsic immune response in comparison to lumenal apical
                      infections. We determined that this asymmetric immune
                      response is driven by the clathrin-sorting adaptor AP-1B,
                      which mediates the polarized sorting of Toll-like receptor 3
                      (TLR3) towards the basolateral side of IECs. Mice and human
                      IECs lacking AP-1B showed an exacerbated immune response
                      following apical stimulation. Together, these results
                      suggest a model where the cellular polarity program plays an
                      integral role in the ability of IECs to partially tolerate
                      apical commensals while remaining fully responsive to
                      invasive basolateral pathogens.},
      cin          = {F140 / C060},
      ddc          = {570},
      cid          = {I:(DE-He78)F140-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31686029},
      doi          = {10.1038/s41564-019-0594-3},
      url          = {https://inrepo02.dkfz.de/record/148628},
}