ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms

Tiffany Bouchery; Ryan Kyle; Mali Camberis; Amy Shepherd; Kara Filbey; Alexander Smith; Marina Harvie; Gavin Painter; Karen Johnston; Peter Ferguson; Rohit Jain; Ben Roediger; Brett Delahunt; Wolfgang Weninger; Elizabeth Forbes-Blom; Graham Le Gros

doi:10.1038/ncomms7970

ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms

Tiffany Bouchery, Ryan Kyle, Mali Camberis, Amy Shepherd, Kara Filbey, Alexander Smith, Marina Harvie, Gavin Painter, Karen Johnston, Peter Ferguson, Rohit Jain, Ben Roediger, Brett Delahunt, Wolfgang Weninger, Elizabeth Forbes-Blom, Graham Le Gros

Division of Immunology, Immunity to Infection and Respiratory Medicine

Research output: Contribution to journal › Article › peer-review

Abstract

Defining the immune mechanisms underlying protective immunity to helminth infection remains an important challenge. Here we report that lung CD4+ T cells and Group 2 innate lymphoid cells (ILC2s) work in concert to block Nippostrongylus brasiliensis (Nb) development in the parenchyma within 48 h in mice. Immune-damaged larvae have a striking morphological defect that is dependent on the expansion of IL-13-producing ILC2 and CD4+ T cells, and the activation of M2 macrophages. This T-cell requirement can be bypassed by administration of IL-2 or IL-33, resulting in expansion of IL-13-producing ILC2s and larval killing. Depletion of ILC2s inhibits larval killing in IL-2-treated mice. Our results broaden understanding of ILC2’s role in immunity to helminths by demonstrating that they not only act as alarmin sensors, but can also be sustained by CD4+ T cells, ensuring both the prompt activation and the maintenance of IL-13-dependent M2 macrophage immunity in the lung.

Original language	English
Article number	6970
Pages (from-to)	1-13
Number of pages	13
Journal	Nature Communications
Volume	6
DOIs	https://doi.org/10.1038/ncomms7970
Publication status	Published - 27 Apr 2015

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Bouchery, T., Kyle, R., Camberis, M., Shepherd, A., Filbey, K., Smith, A., Harvie, M., Painter, G., Johnston, K., Ferguson, P., Jain, R., Roediger, B., Delahunt, B., Weninger, W., Forbes-Blom, E., & Gros, G. L. (2015). ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms. Nature Communications, 6, 1-13. Article 6970. https://doi.org/10.1038/ncomms7970

@article{6a1f6330ea7e4f129e056b57c4d3a5ed,

title = "ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms",

abstract = "Defining the immune mechanisms underlying protective immunity to helminth infection remains an important challenge. Here we report that lung CD4+ T cells and Group 2 innate lymphoid cells (ILC2s) work in concert to block Nippostrongylus brasiliensis (Nb) development in the parenchyma within 48 h in mice. Immune-damaged larvae have a striking morphological defect that is dependent on the expansion of IL-13-producing ILC2 and CD4+ T cells, and the activation of M2 macrophages. This T-cell requirement can be bypassed by administration of IL-2 or IL-33, resulting in expansion of IL-13-producing ILC2s and larval killing. Depletion of ILC2s inhibits larval killing in IL-2-treated mice. Our results broaden understanding of ILC2{\textquoteright}s role in immunity to helminths by demonstrating that they not only act as alarmin sensors, but can also be sustained by CD4+ T cells, ensuring both the prompt activation and the maintenance of IL-13-dependent M2 macrophage immunity in the lung.",

author = "Tiffany Bouchery and Ryan Kyle and Mali Camberis and Amy Shepherd and Kara Filbey and Alexander Smith and Marina Harvie and Gavin Painter and Karen Johnston and Peter Ferguson and Rohit Jain and Ben Roediger and Brett Delahunt and Wolfgang Weninger and Elizabeth Forbes-Blom and Gros, {Graham Le}",

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journal = "Nature Communications",

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Bouchery, T, Kyle, R, Camberis, M, Shepherd, A, Filbey, K, Smith, A, Harvie, M, Painter, G, Johnston, K, Ferguson, P, Jain, R, Roediger, B, Delahunt, B, Weninger, W, Forbes-Blom, E & Gros, GL 2015, 'ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms', Nature Communications, vol. 6, 6970, pp. 1-13. https://doi.org/10.1038/ncomms7970

TY - JOUR

T1 - ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms

AU - Bouchery, Tiffany

AU - Kyle, Ryan

AU - Camberis, Mali

AU - Shepherd, Amy

AU - Filbey, Kara

AU - Smith, Alexander

AU - Harvie, Marina

AU - Painter, Gavin

AU - Johnston, Karen

AU - Ferguson, Peter

AU - Jain, Rohit

AU - Roediger, Ben

AU - Delahunt, Brett

AU - Weninger, Wolfgang

AU - Forbes-Blom, Elizabeth

AU - Gros, Graham Le

PY - 2015/4/27

Y1 - 2015/4/27

N2 - Defining the immune mechanisms underlying protective immunity to helminth infection remains an important challenge. Here we report that lung CD4+ T cells and Group 2 innate lymphoid cells (ILC2s) work in concert to block Nippostrongylus brasiliensis (Nb) development in the parenchyma within 48 h in mice. Immune-damaged larvae have a striking morphological defect that is dependent on the expansion of IL-13-producing ILC2 and CD4+ T cells, and the activation of M2 macrophages. This T-cell requirement can be bypassed by administration of IL-2 or IL-33, resulting in expansion of IL-13-producing ILC2s and larval killing. Depletion of ILC2s inhibits larval killing in IL-2-treated mice. Our results broaden understanding of ILC2’s role in immunity to helminths by demonstrating that they not only act as alarmin sensors, but can also be sustained by CD4+ T cells, ensuring both the prompt activation and the maintenance of IL-13-dependent M2 macrophage immunity in the lung.

AB - Defining the immune mechanisms underlying protective immunity to helminth infection remains an important challenge. Here we report that lung CD4+ T cells and Group 2 innate lymphoid cells (ILC2s) work in concert to block Nippostrongylus brasiliensis (Nb) development in the parenchyma within 48 h in mice. Immune-damaged larvae have a striking morphological defect that is dependent on the expansion of IL-13-producing ILC2 and CD4+ T cells, and the activation of M2 macrophages. This T-cell requirement can be bypassed by administration of IL-2 or IL-33, resulting in expansion of IL-13-producing ILC2s and larval killing. Depletion of ILC2s inhibits larval killing in IL-2-treated mice. Our results broaden understanding of ILC2’s role in immunity to helminths by demonstrating that they not only act as alarmin sensors, but can also be sustained by CD4+ T cells, ensuring both the prompt activation and the maintenance of IL-13-dependent M2 macrophage immunity in the lung.

U2 - 10.1038/ncomms7970

DO - 10.1038/ncomms7970

M3 - Article

SN - 2041-1723

VL - 6

SP - 1

EP - 13

JO - Nature Communications

JF - Nature Communications

M1 - 6970

ER -

ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms

Abstract

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