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

Laura Campbell, Matthew Hepworth, Jayde Whittingham-Dowd, Seona Thompson, Allison Bancroft, Kelly Hayes, Tovah Shaw, Burton F. Dickey, Anne-Laure Flammar, David Artis, David A. Schwartz, Christopher M. Evans, Ian Roberts, David Thornton, Richard Grencis

Research output: Contribution to journalArticlepeer-review


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 innate driven priming of mucus barriers may have evolved to protect from subsequent infections with multiple helminth species, which occur naturally in endemic areas.
Original languageEnglish
Pages (from-to)2714–2723
JournalJournal of Experimental Medicine
Issue number12
Early online date3 Oct 2019
Publication statusPublished - 2019


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