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@ARTICLE{Gabele:299791,
      author       = {A. Gabele and M. Sprang and M. Cihan and M. Welzel and A.
                      Nurbekova and K. Romaniuk and S. Dietzen and M. Klein and G.
                      Bündgen and M. Emelianov and G. Harms and K. Rajalingam and
                      T. Ziesmann and K. Pape and B. Wasser and D.
                      Gomez-Zepeda$^*$ and K. Braband and M. Delacher and N.
                      Lemmermann and S. Bittner and M. A. Andrade-Navarro and S.
                      Tenzer$^*$ and K. Luck and T. Bopp and U. Distler},
      title        = {{U}nveiling {IRF}4-steered regulation of context-dependent
                      effector programs in {CD}4+ {T} cells under {T}h17- and
                      {T}reg-skewing conditions.},
      journal      = {Cell reports},
      volume       = {44},
      number       = {3},
      issn         = {2211-1247},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2025-00546},
      pages        = {115407},
      year         = {2025},
      note         = {HI-TRON},
      abstract     = {The transcription factor interferon regulatory factor 4
                      (IRF4) is crucial for the fate determination of
                      pro-inflammatory T helper (Th) 17 and the functionally
                      opposing group of immunomodulatory regulatory T (Treg)
                      cells. However, the molecular mechanisms of how IRF4 steers
                      diverse transcriptional programs in Th17 and Treg cells are
                      far from being definitive. Here, we integrated data derived
                      from affinity-purification and full mass-spectrometry-based
                      proteome analysis with chromatin immunoprecipitation
                      sequencing. This allowed the characterization of
                      subtype-specific molecular programs and the identification
                      of IRF4 interactors in the Th17/Treg context. Our data
                      reveal that IRF4-interacting transcription factors are
                      recruited to IRF composite elements for the regulation of
                      cell-type-specific transcriptional programs as exemplarily
                      demonstrated for FLI1, which, in cooperation with IRF4,
                      promotes Th17-specific gene expression. FLI1 inhibition
                      markedly impaired Th17 differentiation. The present 'omics'
                      dataset provides a valuable resource for studying
                      IRF4-mediated gene regulatory programs in pro- and
                      anti-inflammatory immune responses.},
      keywords     = {CP: Immunology (Other) / ChIP-seq (Other) / FLI1 (Other) /
                      IRF4 (Other) / Th17 cells (Other) / Treg cells (Other) /
                      composite motif (Other) / protein-protein interaction
                      (Other) / proteomics (Other)},
      cin          = {D190 / D191},
      ddc          = {610},
      cid          = {I:(DE-He78)D190-20160331 / I:(DE-He78)D191-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40067830},
      doi          = {10.1016/j.celrep.2025.115407},
      url          = {https://inrepo02.dkfz.de/record/299791},
}