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

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites. / Campbell, Laura; Hepworth, Matthew R; Whittingham-Dowd, Jayde et al.
In: The Journal of experimental medicine, Vol. 216, No. 12, 02.12.2019, p. 2714-2723.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Campbell, L, Hepworth, MR, Whittingham-Dowd, J, Thompson, S, Bancroft, AJ, Hayes, KS, Shaw, TN, Dickey, BF, Flamar, A-L, Artis, D, Schwartz, DA, Evans, CM, Roberts, IS, Thornton, DJ & Grencis, RK 2019, 'ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites', The Journal of experimental medicine, vol. 216, no. 12, pp. 2714-2723. https://doi.org/10.1084/jem.20180610

APA

Campbell, L., Hepworth, M. R., Whittingham-Dowd, J., Thompson, S., Bancroft, A. J., Hayes, K. S., Shaw, T. N., Dickey, B. F., Flamar, A-L., Artis, D., Schwartz, D. A., Evans, C. M., Roberts, I. S., Thornton, D. J., & Grencis, R. K. (2019). ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites. The Journal of experimental medicine, 216(12), 2714-2723. https://doi.org/10.1084/jem.20180610

Vancouver

Campbell L, Hepworth MR, Whittingham-Dowd J, Thompson S, Bancroft AJ, Hayes KS et al. ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites. The Journal of experimental medicine. 2019 Dec 2;216(12):2714-2723. Epub 2019 Oct 3. doi: 10.1084/jem.20180610

Author

Campbell, Laura ; Hepworth, Matthew R ; Whittingham-Dowd, Jayde et al. / ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites. In: The Journal of experimental medicine. 2019 ; Vol. 216, No. 12. pp. 2714-2723.

Bibtex

@article{f897ef20217e4b6d9135f62de600f449,
title = "ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites",
abstract = "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.",
author = "Laura Campbell and Hepworth, {Matthew R} and Jayde Whittingham-Dowd and Seona Thompson and Bancroft, {Allison J} and Hayes, {Kelly S} and Shaw, {Tovah N} and Dickey, {Burton F} and Anne-Laure Flamar and David Artis and Schwartz, {David A} and Evans, {Christopher M} and Roberts, {Ian S} and Thornton, {David J} and Grencis, {Richard K}",
note = "{\textcopyright} 2019 Campbell et al.",
year = "2019",
month = dec,
day = "2",
doi = "10.1084/jem.20180610",
language = "English",
volume = "216",
pages = "2714--2723",
journal = "The Journal of experimental medicine",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "12",

}

RIS

TY - JOUR

T1 - ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites

AU - Campbell, Laura

AU - Hepworth, Matthew R

AU - Whittingham-Dowd, Jayde

AU - Thompson, Seona

AU - Bancroft, Allison J

AU - Hayes, Kelly S

AU - Shaw, Tovah N

AU - Dickey, Burton F

AU - Flamar, Anne-Laure

AU - Artis, David

AU - Schwartz, David A

AU - Evans, Christopher M

AU - Roberts, Ian S

AU - Thornton, David J

AU - Grencis, Richard K

N1 - © 2019 Campbell et al.

PY - 2019/12/2

Y1 - 2019/12/2

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 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.

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 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.

U2 - 10.1084/jem.20180610

DO - 10.1084/jem.20180610

M3 - Journal article

C2 - 31582416

VL - 216

SP - 2714

EP - 2723

JO - The Journal of experimental medicine

JF - The Journal of experimental medicine

SN - 0022-1007

IS - 12

ER -