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@ARTICLE{Khne:279433,
      author       = {Köhne, Maren and Shakiba, Mehrnoush Hadaddzadeh and
                      Schmidleithner, Lisa and Schulte-Schrepping, Jonas and
                      Scholz, Rebekka and Elmzzahi, Tarek and Sommer, Daniel and
                      Li, Yuanfang and Carraro, Caterina and De Domenico, Elena
                      and Wißfeld, Jannis and Händler, Kristian and Hamada, Doaa
                      and Frolov, Aleksej and Cheng, Xiaoxiao and Baumgart,
                      Ann-Kathrin and Holsten, Lisa and Osei-Sarpong, Collins and
                      Bourry, Svenja and Thabet, Yasser and Renken, Hannes and
                      Paulusch, Stefan and Sadlon, Timothy and Buch, Thorsten and
                      Wunderlich, F Thomas and Wickenhauser, Claudia and Alferink,
                      Judith and Kuhlmann, Tanja and Geyer, Matthias and Bonaguro,
                      Lorenzo and Barry, Simon C and Schultze, Joachim L and
                      Beyer, Marc D},
      title        = {{S}atb1 directs the differentiation of {TH}17 cells through
                      suppression of {IL}-2 expression.},
      journal      = {Cell reports},
      volume       = {44},
      number       = {7},
      issn         = {2211-1247},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DZNE-2025-00764},
      pages        = {115866},
      year         = {2025},
      abstract     = {T helper (TH)17 cells are crucial for host defense in
                      barrier organs, and their altered functionality can disrupt
                      tissue homeostasis, increasing the risk of autoimmune
                      diseases. Thus, it is essential to understand the mechanisms
                      controlling TH17 differentiation to develop strategies
                      influencing their role in diseases. Here, we identified
                      Special AT-rich sequence-binding protein 1 (Satb1) as a
                      pioneering factor for TH17 development. Satb1 is highly
                      expressed in TH17 cells, and loss of Satb1 prevents the
                      differentiation of TH17 cells. Consequently, expression of
                      Satb1 in CD4+ T cells is required for the formation of
                      TH17-driven autoimmune diseases. Mechanistically, Satb1
                      mediates TH17 development through regulating accessibility
                      of the Il2 gene locus and thereby preventing interleukin
                      (IL)-2 signaling early during TH17 differentiation. Hence,
                      suppression of IL-2 expression by Satb1 during TH17
                      formation is pivotal, suggesting that Satb1 could serve as a
                      novel therapeutic target for treating autoimmune diseases
                      driven by TH17 cells.},
      keywords     = {CD4(+) T cell differentiation (Other) / CP: Immunology
                      (Other) / EAE (Other) / IL-2 (Other) / Satb1 (Other) /
                      T(H)17 cells (Other) / autoimmune disease (Other) / colitis
                      (Other) / scRNA-seq (Other) / single-cell MultiOMICs
                      (Other)},
      cin          = {AG Beyer / AG Schultze / AG Bonaguro},
      ddc          = {610},
      cid          = {I:(DE-2719)1013035 / I:(DE-2719)1013038 /
                      I:(DE-2719)1016005},
      pnm          = {351 - Brain Function (POF4-351) / 354 - Disease Prevention
                      and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40531625},
      doi          = {10.1016/j.celrep.2025.115866},
      url          = {https://pub.dzne.de/record/279433},
}