TY - JOUR
T1 - ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites
AU - Campbell, Laura
AU - Hepworth, Matthew
AU - Whittingham-Dowd, Jayde
AU - Thompson, Seona
AU - Bancroft, Allison
AU - Hayes, Kelly
AU - Shaw, Tovah
AU - Dickey, Burton F.
AU - Flammar, Anne-Laure
AU - Artis, David
AU - Schwartz, David A.
AU - Evans, Christopher M.
AU - Roberts, Ian
AU - Thornton, David
AU - Grencis, Richard
PY - 2019
Y1 - 2019
N2 - 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.
AB - 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.
U2 - 10.1084/jem.20180610
DO - 10.1084/jem.20180610
M3 - Article
SN - 0022-1007
VL - 216
SP - 2714
EP - 2723
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
IS - 12
ER -