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 and Graham Le Gros ()
Additional contact information
Tiffany Bouchery: Malaghan Institute of Medical Research
Ryan Kyle: Malaghan Institute of Medical Research
Mali Camberis: Malaghan Institute of Medical Research
Amy Shepherd: Malaghan Institute of Medical Research
Kara Filbey: Malaghan Institute of Medical Research
Alexander Smith: Malaghan Institute of Medical Research
Marina Harvie: Queensland University of Technology
Gavin Painter: The Ferrier Research Institute, Victoria University of Wellington, Lower Hutt
Karen Johnston: The Ferrier Research Institute, Victoria University of Wellington, Lower Hutt
Peter Ferguson: University of Otago
Rohit Jain: The Centenary Institute
Ben Roediger: The Centenary Institute
Brett Delahunt: University of Otago
Wolfgang Weninger: The Centenary Institute
Elizabeth Forbes-Blom: Malaghan Institute of Medical Research
Graham Le Gros: Malaghan Institute of Medical Research

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms7970

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