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

T Bouchery, R Kyle, M Camberis, A Shepherd… - Nature …, 2015 - nature.com
T Bouchery, R Kyle, M Camberis, A Shepherd, K Filbey, A Smith, M Harvie, G Painter
Nature communications, 2015nature.com
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 …
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.
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