| First Author | Campbell L | Year | 2019 |
| Journal | J Exp Med | Volume | 216 |
| Issue | 12 | Pages | 2714-2723 |
| PubMed ID | 31582416 | Mgi Jnum | J:285101 |
| Mgi Id | MGI:6392453 | Doi | 10.1084/jem.20180610 |
| Citation | Campbell L, et al. (2019) ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites. J Exp Med 216(12):2714-2723 |
| abstractText | 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. |
