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@ARTICLE{Deshpande:304981,
      author       = {D. Deshpande and L. Velleman and J. Schmitz and P. M.
                      Forster and C. Schinke and S. Boulekou and H. P. Düsedau
                      and S. M. Krug and T. Mertens and X. Gao and C. Figueiredo
                      and K. J. Jarick and T. Plum$^*$ and N. Sterczyk and P. S.
                      Leclère and S. Helfrich and A. Tappe-Theodor and K. Kotsch
                      and J. Steffen and D. Voehringer and C. U. Duerr and A. E.
                      Hauser and D. Artis and C. Pitzer and I. R. Dunay and C. S.
                      N. Klose},
      title        = {{G}roup 2 innate lymphoid cells regulate nociceptive and
                      gait functions of the peripheral nervous system.},
      journal      = {Science immunology},
      volume       = {10},
      number       = {111},
      issn         = {2470-9468},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DKFZ-2025-01972},
      pages        = {eadp7092},
      year         = {2025},
      abstract     = {The peripheral nervous system (PNS) is involved in
                      nociception and gait. The contribution of PNS-resident
                      immune cells to these functions is not fully understood. We
                      identified group 2 innate lymphoid cells (ILC2s) as a
                      distinct immune cell population resident in the PNS, with a
                      unique gene profile facilitating neuron-ILC2 cross-talk.
                      ILC2-deficient mice display PNS dysfunction
                      (hypersensitivity and gait anomalies). These functional
                      deficits are attributed to structural abnormalities in the
                      sciatic nerves of ILC2-deficient mice. ILC2s communicate
                      with dorsal root ganglion neurons via the interleukin-13
                      (IL-13) signaling pathway to maintain nerve structure and
                      pain thresholds. Loss of the shared IL-4/IL-13 receptor
                      (IL-4R/IL-13R) in neurons results in a phenotype similar to
                      ILC2-deficient mice. Intrathecally administered IL-13
                      rescues hypersensitivity and gait defects in ILC2-deficient
                      mice, which suggests that this signaling pathway may be
                      therapeutically important. This work therefore identifies a
                      function for ILC2s in regulating the nerve structural
                      integrity and nociceptive functions of the PNS.},
      keywords     = {Animals / Mice / Immunity, Innate / Mice, Knockout /
                      Lymphocytes: immunology / Gait: immunology / Peripheral
                      Nervous System: immunology / Mice, Inbred C57BL /
                      Interleukin-13: immunology / Nociception / Male / Ganglia,
                      Spinal: immunology / Signal Transduction / Interleukin-13
                      (NLM Chemicals)},
      cin          = {D110},
      ddc          = {610},
      cid          = {I:(DE-He78)D110-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41004566},
      doi          = {10.1126/sciimmunol.adp7092},
      url          = {https://inrepo02.dkfz.de/record/304981},
}