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ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites

Research output: Contribution to journalJournal articlepeer-review

  • Laura Campbell
  • Matthew R Hepworth
  • Jayde Whittingham-Dowd
  • Seona Thompson
  • Allison J Bancroft
  • Kelly S Hayes
  • Tovah N Shaw
  • Burton F Dickey
  • Anne-Laure Flamar
  • David Artis
  • David A Schwartz
  • Christopher M Evans
  • Ian S Roberts
  • David J Thornton
  • Richard K Grencis
<mark>Journal publication date</mark>2/12/2019
<mark>Journal</mark>The Journal of experimental medicine
Issue number12
Number of pages10
Pages (from-to)2714-2723
Publication StatusPublished
Early online date3/10/19
<mark>Original language</mark>English


Host immunity to parasitic nematodes requires the generation of a robust type 2 cytokine response, characterized by the production of interleukin 13 (IL-13), which drives expulsion. Here, we show that infection with helminths in the intestine also induces an ILC2-driven, IL-13-dependent goblet cell hyperplasia and increased production of mucins (Muc5b and Muc5ac) at distal sites, including the lungs and other mucosal barrier sites. Critically, we show that type 2 priming of lung tissue through increased mucin production inhibits the progression of a subsequent lung migratory helminth infection and limits its transit through the airways. These data show that infection by gastrointestinal-dwelling helminths induces a systemic innate mucin response that primes peripheral barrier sites for protection against subsequent secondary helminth infections. These data suggest that innate-driven priming of mucus barriers may have evolved to protect from subsequent infections with multiple helminth species, which occur naturally in endemic areas.

Bibliographic note

© 2019 Campbell et al.