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@ARTICLE{Plum:277476,
      author       = {T. Plum$^*$ and R. Binzberger$^*$ and R. Thiele$^*$ and F.
                      Shang$^*$ and D. Postrach$^*$ and C. Fung and M. Fortea and
                      N. Stakenborg and Z. Wang and A. Tappe-Theodor and T. Poth
                      and D. MacLaren$^*$ and G. Boeckxstaens and R. Kuner and C.
                      Pitzer and H. Monyer$^*$ and C. Xin and J. V. Bonventre and
                      S. Tanaka and D. Voehringer and P. V. Berghe and J. Strid
                      and T. Feyerabend$^*$ and H.-R. Rodewald$^*$},
      title        = {{M}ast cells link immune sensing to antigen-avoidance
                      behaviour.},
      journal      = {Nature},
      volume       = {620},
      number       = {7974},
      issn         = {0028-0836},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2023-01397},
      pages        = {634-642},
      year         = {2023},
      note         = {#EA:D110#LA:D110# / 2023 Aug;620(7974):634-642},
      abstract     = {The physiological functions of mast cells remain largely an
                      enigma. In the context of barrier damage, mast cells are
                      integrated in type 2 immunity and, together with
                      immunoglobulin E (IgE), promote allergic diseases. Allergic
                      symptoms may, however, facilitate expulsion of allergens,
                      toxins and parasites and trigger future antigen
                      avoidance1-3. Here, we show that antigen-specific avoidance
                      behaviour in inbred mice4,5 is critically dependent on mast
                      cells; hence, we identify the immunological sensor cell
                      linking antigen recognition to avoidance behaviour.
                      Avoidance prevented antigen-driven adaptive, innate and
                      mucosal immune activation and inflammation in the stomach
                      and small intestine. Avoidance was IgE dependent, promoted
                      by Th2 cytokines in the immunization phase and by IgE in the
                      execution phase. Mucosal mast cells lining the stomach and
                      small intestine rapidly sensed antigen ingestion. We
                      interrogated potential signalling routes between mast cells
                      and the brain using mutant mice, pharmacological inhibition,
                      neural activity recordings and vagotomy. Inhibition of
                      leukotriene synthesis impaired avoidance, but overall no
                      single pathway interruption completely abrogated avoidance,
                      indicating complex regulation. Collectively, the stage for
                      antigen avoidance is set when adaptive immunity equips mast
                      cells with IgE as a telltale of past immune responses. On
                      subsequent antigen ingestion, mast cells signal termination
                      of antigen intake. Prevention of immunopathology-causing,
                      continuous and futile responses against per se innocuous
                      antigens or of repeated ingestion of toxins through
                      mast-cell-mediated antigen-avoidance behaviour may be an
                      important arm of immunity.},
      cin          = {D110 / A230},
      ddc          = {500},
      cid          = {I:(DE-He78)D110-20160331 / I:(DE-He78)A230-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37438525},
      doi          = {10.1038/s41586-023-06188-0},
      url          = {https://inrepo02.dkfz.de/record/277476},
}