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@ARTICLE{Chang:268493,
      author       = {Chang, Yinshui and Bach, Luisa and Hasiuk, Marko and Wen,
                      Lifen and Elmzzahi, Tarek and Tsui, Carlson and
                      Gutiérrez-Melo, Nicolás and Steffen, Teresa and
                      Utzschneider, Daniel T and Raj, Timsse and Jost, Paul Jonas
                      and Heink, Sylvia and Cheng, Jingyuan and Burton, Oliver T
                      and Zeiträg, Julia and Alterauge, Dominik and Dahlström,
                      Frank and Becker, Jennifer-Christin and Kastl, Melanie and
                      Symeonidis, Konstantinos and van Uelft, Martina and Becker,
                      Matthias Kai Holger and Reschke, Sarah and Krebs, Stefan and
                      Blum, Helmut and Abdullah, Zeinab and Paeschke, Katrin and
                      Ohnmacht, Caspar and Neumann, Christian and Liston, Adrian
                      and Meissner, Felix and Korn, Thomas and Hasenauer, Jan and
                      Heissmeyer, Vigo and Beyer, Marc-Daniel and Kallies, Axel
                      and Jeker, Lukas T and Baumjohann, Dirk},
      title        = {{TGF}-β specifies {TFH} versus {TH}17 cell fates in murine
                      {CD}4+ {T} cells through c-{M}af.},
      journal      = {Science immunology},
      volume       = {9},
      number       = {93},
      issn         = {2470-9468},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DZNE-2024-00239},
      pages        = {eadd4818},
      year         = {2024},
      abstract     = {T follicular helper (TFH) cells are essential for effective
                      antibody responses, but deciphering the intrinsic wiring of
                      mouse TFH cells has long been hampered by the lack of a
                      reliable protocol for their generation in vitro. We report
                      that transforming growth factor-β (TGF-β) induces robust
                      expression of TFH hallmark molecules CXCR5 and Bcl6 in
                      activated mouse CD4+ T cells in vitro. TGF-β-induced mouse
                      CXCR5+ TFH cells are phenotypically, transcriptionally, and
                      functionally similar to in vivo-generated TFH cells and
                      provide critical help to B cells. The study further reveals
                      that TGF-β-induced CXCR5 expression is independent of Bcl6
                      but requires the transcription factor c-Maf. Classical
                      TGF-β-containing T helper 17 (TH17)-inducing conditions
                      also yield separate CXCR5+ and IL-17A-producing cells,
                      highlighting shared and distinct cell fate trajectories of
                      TFH and TH17 cells. We demonstrate that excess IL-2 in
                      high-density T cell cultures interferes with the
                      TGF-β-induced TFH cell program, that TFH and TH17 cells
                      share a common developmental stage, and that c-Maf acts as a
                      switch factor for TFH versus TH17 cell fates in TGF-β-rich
                      environments in vitro and in vivo.},
      keywords     = {Animals / Mice / T-Lymphocytes, Helper-Inducer /
                      Transforming Growth Factor beta: metabolism / B-Lymphocytes
                      / CD4-Positive T-Lymphocytes / Cell Differentiation /
                      Proto-Oncogene Proteins c-maf: metabolism / Transforming
                      Growth Factor beta (NLM Chemicals) / Maf protein, mouse (NLM
                      Chemicals) / Proto-Oncogene Proteins c-maf (NLM Chemicals)},
      cin          = {AG Beyer / AG Becker / PRECISE},
      ddc          = {610},
      cid          = {I:(DE-2719)1013035 / I:(DE-2719)5000079 /
                      I:(DE-2719)1013031},
      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},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38427718},
      doi          = {10.1126/sciimmunol.add4818},
      url          = {https://pub.dzne.de/record/268493},
}