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

Research output: Contribution to journalArticlepeer-review


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 languageEnglish
Article number6970
Pages (from-to)1-13
Number of pages13
JournalNature Communications
Publication statusPublished - 27 Apr 2015


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