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@ARTICLE{Michel:130957,
      author       = {C. Michel$^*$ and C. N. Miller and R. Küchler$^*$ and B.
                      Brors$^*$ and M. S. Anderson and B. Kyewski$^*$ and S.
                      Pinto$^*$},
      title        = {{R}evisiting the {R}oad {M}ap of {M}edullary {T}hymic
                      {E}pithelial {C}ell {D}ifferentiation.},
      journal      = {The journal of immunology},
      volume       = {199},
      number       = {10},
      issn         = {1550-6606},
      address      = {Bethesda, Md.},
      publisher    = {Soc.},
      reportid     = {DKFZ-2017-06033},
      pages        = {3488 - 3503},
      year         = {2017},
      abstract     = {The basic two-step terminal differentiation model of the
                      medullary thymic epithelial cell (mTEC) lineage from
                      immature MHC class II (MHCII)(lo) to mature MHCII(hi) mTECs
                      has recently been extended to include a third stage, namely
                      the post-Aire MHCII(lo) subset as identified by
                      lineage-tracing models. However, a suitable surface marker
                      distinguishing the phenotypically overlapping pre- from the
                      post-Aire MHCII(lo) stage has been lacking. In this study,
                      we introduce the lectin Tetragonolobus purpureas agglutinin
                      (TPA) as a novel cell surface marker that allows for such
                      delineation. Based on our data, we derived the following
                      sequence of mTEC differentiation: TPA(lo)MHCII(lo) →
                      TPA(lo)MHCII(hi) → TPA(hi)MHCII(hi) → TPA(hi)MHCII(lo)
                      Surprisingly, in the steady-state postnatal thymus
                      TPA(lo)MHCII(lo) pre-Aire rather than terminally
                      differentiated post-Aire TPA(hi)MHCII(lo) mTECs were marked
                      for apoptosis at an exceptionally high rate of $∼70\%.$
                      Hence, only the minor cycling fraction of the MHCII(lo)
                      subset $(<20\%)$ potentially qualified as mTEC precursors.
                      FoxN1 expression inversely correlated with the fraction of
                      slow cycling and apoptotic cells within the four TPA
                      subsets. TPA also further subdivided human mTECs, although
                      with different subset distribution. Our revised road map
                      emphazises close parallels of terminal mTEC development with
                      that of skin, undergoing an alternative route of cell death,
                      namely cornification rather than apoptosis. The high rate of
                      apoptosis in pre-Aire MHCII(lo) mTECs points to a 'quality
                      control' step during early mTEC differentiation.},
      cin          = {D090 ; D090 / G200 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)D090-20160331 / I:(DE-He78)G200-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28993517},
      doi          = {10.4049/jimmunol.1700203},
      url          = {https://inrepo02.dkfz.de/record/130957},
}