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

Author

Listed:
  • Tiffany Bouchery

    (Malaghan Institute of Medical Research)

  • Ryan Kyle

    (Malaghan Institute of Medical Research
    School of Biological Sciences, Victoria University of Wellington)

  • 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
    Discipline of Dermatology, Sydney Medical School)

  • Ben Roediger

    (The Centenary Institute
    Discipline of Dermatology, Sydney Medical School)

  • Brett Delahunt

    (University of Otago)

  • Wolfgang Weninger

    (The Centenary Institute
    Discipline of Dermatology, Sydney Medical School
    Royal Prince Alfred Hospital)

  • Elizabeth Forbes-Blom

    (Malaghan Institute of Medical Research)

  • Graham Le Gros

    (Malaghan Institute of Medical Research)

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.

Suggested Citation

  • 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 Delahu, 2015. "ILC2s and T cells cooperate to ensure maintenance of M2 macrophages for lung immunity against hookworms," Nature Communications, Nature, vol. 6(1), pages 1-13, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7970
    DOI: 10.1038/ncomms7970
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    Cited by:

    1. Sang Hun Lee & Byunghyun Kang & Olena Kamenyeva & Tiago Rodrigues Ferreira & Kyoungin Cho & Jaspal S. Khillan & Juraj Kabat & Brian L. Kelsall & David L. Sacks, 2023. "Dermis resident macrophages orchestrate localized ILC2 eosinophil circuitries to promote non-healing cutaneous leishmaniasis," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    2. Juliane Glaubitz & Anika Wilden & Janine Golchert & Georg Homuth & Uwe Völker & Barbara M. Bröker & Thomas Thiele & Markus M. Lerch & Julia Mayerle & Ali A. Aghdassi & Frank U. Weiss & Matthias Sendle, 2022. "In mouse chronic pancreatitis CD25+FOXP3+ regulatory T cells control pancreatic fibrosis by suppression of the type 2 immune response," Nature Communications, Nature, vol. 13(1), pages 1-20, December.

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