A mast cell-ILC2-Th9 pathway promotes lung inflammation in cystic fibrosis

نویسندگان

  • Silvia Moretti
  • Giorgia Renga
  • Vasilis Oikonomou
  • Claudia Galosi
  • Marilena Pariano
  • Rossana G Iannitti
  • Monica Borghi
  • Matteo Puccetti
  • Marco De Zuani
  • Carlo E Pucillo
  • Giuseppe Paolicelli
  • Teresa Zelante
  • Jean-Christophe Renauld
  • Oxana Bereshchenko
  • Paolo Sportoletti
  • Vincenzina Lucidi
  • Maria Chiara Russo
  • Carla Colombo
  • Ersilia Fiscarelli
  • Cornelia Lass-Flörl
  • Fabio Majo
  • Gabriella Ricciotti
  • Helmut Ellemunter
  • Luigi Ratclif
  • Vincenzo Nicola Talesa
  • Valerio Napolioni
  • Luigina Romani
چکیده

T helper 9 (Th9) cells contribute to lung inflammation and allergy as sources of interleukin-9 (IL-9). However, the mechanisms by which IL-9/Th9 mediate immunopathology in the lung are unknown. Here we report an IL-9-driven positive feedback loop that reinforces allergic inflammation. We show that IL-9 increases IL-2 production by mast cells, which leads to expansion of CD25+ type 2 innate lymphoid cells (ILC2) and subsequent activation of Th9 cells. Blocking IL-9 or inhibiting CD117 (c-Kit) signalling counteracts the pathogenic effect of the described IL-9-mast cell-IL-2 signalling axis. Overproduction of IL-9 is observed in expectorates from cystic fibrosis (CF) patients, and a sex-specific variant of IL-9 is predictive of allergic reactions in female patients. Our results suggest that blocking IL-9 may be a therapeutic strategy to ameliorate inflammation associated with microbial colonization in the lung, and offers a plausible explanation for gender differences in clinical outcomes of patients with CF.

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عنوان ژورنال:

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2017