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@ARTICLE{Barilla:301545,
      author       = {R. M. Barilla and C. Berard and L. Sun and S. Sandhu and S.
                      Zaghouani and K. S. Iyer and G. Altun$^*$ and C.-W. Su and
                      J. Deguine and V. Singh and Y. Hou and K. Kusumakar and M.
                      L. Rutlin and M. Rao and H. Zaghouani and H. N. Shi and R.
                      J. Xavier and V. K. Kuchroo},
      title        = {{T}ype 2 cytokines act on enteric sensory neurons to
                      regulate neuropeptide-driven host defense.},
      journal      = {Science},
      volume       = {389},
      number       = {6757},
      issn         = {0036-8075},
      address      = {Washington, DC},
      publisher    = {American Association for the Advancement of Science},
      reportid     = {DKFZ-2025-01066},
      pages        = {260-267},
      year         = {2025},
      note         = {2025 Jul 17;389(6757):260-267},
      abstract     = {Enteric nervous system (ENS)-derived neuropeptides modulate
                      immune cell function, yet our understanding of how
                      inflammatory cues directly influence enteric neuron
                      responses during infection is considerably lacking. Here, we
                      characterized a primary enteric sensory neuron (PSN) subset
                      producing the neuropeptides neuromedin U (NMU) and
                      calcitonin gene-related peptide β (CGRPβ) and coexpressing
                      receptors for the type 2 cytokines interleukin-4 (IL-4) and
                      IL-13. Type 2 cytokines amplified NMU and CGRPβ expression
                      in PSNs, in vitro and in vivo, which was abrogated by
                      PSN-specific Il13ra1 deletion. Deletion of Il13ra1 in PSNs
                      impaired host defense to the gastrointestinal helminth
                      Heligmosomoides polygyrus and blunted muscularis immune
                      responses. Co-administration of NMU23 and CGRPβ rescued
                      helminth clearance deficits and restored anti-helminth
                      immunity, highlighting the essential bi-directional
                      neuro-immune crosstalk regulating intestinal type 2
                      inflammation.},
      cin          = {B370},
      ddc          = {500},
      cid          = {I:(DE-He78)B370-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40403128},
      doi          = {10.1126/science.adn9850},
      url          = {https://inrepo02.dkfz.de/record/301545},
}