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@ARTICLE{Delacher:143508,
      author       = {M. Delacher$^*$ and C. Schmidl and Y. Herzig and M. Breloer
                      and W. Hartmann and F. Brunk$^*$ and D. Kägebein$^*$ and U.
                      Träger$^*$ and A.-C. Hofer$^*$ and S. Bittner and D.
                      Weichenhan$^*$ and C. D. Imbusch$^*$ and A.
                      Hotz-Wagenblatt$^*$ and T. Hielscher$^*$ and A. Breiling$^*$
                      and G. Federico$^*$ and H.-J. Gröne$^*$ and R. M. Schmid
                      and M. Rehli and J. Abramson and M. Feuerer$^*$},
      title        = {{R}bpj expression in regulatory {T} cells is critical for
                      restraining {TH}2 responses.},
      journal      = {Nature Communications},
      volume       = {10},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2019-01092},
      pages        = {1621},
      year         = {2019},
      abstract     = {The transcriptional regulator Rbpj is involved in T-helper
                      (TH) subset polarization, but its function in Treg cells
                      remains unclear. Here we show that Treg-specific Rbpj
                      deletion leads to splenomegaly and lymphadenopathy despite
                      increased numbers of Treg cells with a polyclonal TCR
                      repertoire. A specific defect of Rbpj-deficient Treg cells
                      in controlling TH2 polarization and B cell responses is
                      observed, leading to the spontaneous formation of germinal
                      centers and a TH2-associated immunoglobulin class switch.
                      The observed phenotype is environment-dependent and can be
                      induced by infection with parasitic nematodes.
                      Rbpj-deficient Treg cells adopt open chromatin landscapes
                      and gene expression profiles reminiscent of tissue-derived
                      TH2-polarized Treg cells, with a prevailing signature of the
                      transcription factor Gata-3. Taken together, our study
                      suggests that Treg cells require Rbpj to specifically
                      restrain TH2 responses, including their own excessive
                      TH2-like differentiation potential.},
      cin          = {D100 / D090 ; D090 / B370 / B330 / W180 / C060 / A130 /
                      G130},
      ddc          = {500},
      cid          = {I:(DE-He78)D100-20160331 / I:(DE-He78)D090-20160331 /
                      I:(DE-He78)B370-20160331 / I:(DE-He78)B330-20160331 /
                      I:(DE-He78)W180-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)A130-20160331 / I:(DE-He78)G130-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30962454},
      pmc          = {pmc:PMC6453958},
      doi          = {10.1038/s41467-019-09276-w},
      url          = {https://inrepo02.dkfz.de/record/143508},
}