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@ARTICLE{Jakob:282558,
      author       = {Jakob, Manuel O and Sterczyk, Nele and Boulekou, Sotiria
                      and Forster, Patrycja M and Barleben, Luisa and Alzain,
                      Nadra and Jarick, Katja J and Pirzgalska, Roksana M and
                      Raposo, Bruno and Hansson, Karl and Nyström, Elisabeth E L
                      and Gondrand, Aurelia and González-Acera, Miguel and
                      Leclère, Pierre S and Lapson, Marlen S and Poggenseier,
                      Sarah and Deshpande, Divija and Velleman, Laura and
                      Breiderhoff, Tilman and Brunkhorst, Max Felix and Schüle,
                      Anton M and Guerra, Gabriela M and Durek, Pawel and
                      Mashreghi, Mir-Farzin and Kühl, Anja A and Chu, Coco and
                      Schneider, Christoph and Weidinger, Carl and Siegmund,
                      Britta and Nordmann, Thierry M and Voehringer, David and
                      Patankar, Jay V and Becker, Christoph and Birchenough,
                      George M H and Veiga-Fernandes, Henrique and Ronchi,
                      Francesca and Kolesnichenko, Marina and Diefenbach, Andreas
                      and Klose, Christoph S N},
      title        = {{E}nteric nervous system-derived {VIP} restrains
                      differentiation of {LGR}5+ stem cells toward the secretory
                      lineage impeding type 2 immune programs.},
      journal      = {Nature immunology},
      volume       = {26},
      number       = {12},
      issn         = {1529-2908},
      address      = {London},
      publisher    = {Springer Nature Limited},
      reportid     = {DZNE-2025-01321},
      pages        = {2227 - 2243},
      year         = {2025},
      abstract     = {Barrier homeostasis relies on a finely tuned interplay
                      between the immune system, epithelial cells and commensal
                      microbiota. Beyond these regulators, the enteric nervous
                      system has recently emerged as a central hub coordinating
                      intestinal immune responses, although its role in epithelial
                      differentiation has remained largely unexplored. Here, we
                      identify a neuroepithelial circuit in which vasoactive
                      intestinal peptide (VIP)-positive enteric neurons act on
                      VIPR1+ epithelial stem cells to restrain both their
                      proliferation and secretory lineage differentiation.
                      Disruption of this pathway leads to an expansion of tuft
                      cells, enhanced interleukin (IL)-25 production, activation
                      of group 2 innate lymphoid cells (ILC2s) and induction of a
                      type 2 immune response resembling worm expulsion. This
                      phenotype occurs independently of the microbiota but is
                      modulated by the IL-25R-ILC2-IL-13 axis and dietary solid
                      food intake. Our findings expose the enteric nervous system
                      as a critical regulator of epithelial fate decisions and
                      immune balance, complementing established mechanisms that
                      safeguard barrier integrity and mucosal homeostasis.},
      keywords     = {Animals / Vasoactive Intestinal Peptide: metabolism /
                      Vasoactive Intestinal Peptide: immunology / Enteric Nervous
                      System: immunology / Enteric Nervous System: metabolism /
                      Cell Differentiation: immunology / Mice / Receptors,
                      G-Protein-Coupled: metabolism / Cell Lineage / Intestinal
                      Mucosa: immunology / Intestinal Mucosa: metabolism /
                      Lymphocytes: immunology / Immunity, Innate / Mice, Inbred
                      C57BL / Stem Cells: immunology / Stem Cells: metabolism /
                      Mice, Knockout / Homeostasis / Vasoactive Intestinal Peptide
                      (NLM Chemicals) / Receptors, G-Protein-Coupled (NLM
                      Chemicals) / Lgr5 protein, mouse (NLM Chemicals)},
      cin          = {AG Wurst},
      ddc          = {610},
      cid          = {I:(DE-2719)1140001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41286457},
      doi          = {10.1038/s41590-025-02325-1},
      url          = {https://pub.dzne.de/record/282558},
}