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Abstract
The early migratory phase of pulmonary helminth infections is characterized by tissue injury leading to the release of the alarmin interleukin (IL)-33 and subsequent induction of type 2 immune responses. We recently described a role for IL-17A, through suppression of interferon (IFN)-γ, as an important inducer of type 2 responses during infection with the lung-migrating rodent nematode Nippostrongylus brasiliensis. Here, we aimed to investigate the interaction between IL-17A and IL-33 during the early lung migratory stages of N. brasiliensis infection. In this brief report, we demonstrate that deficiency of IL-17A leads to impaired IL-33 expression and secretion early in infection, independent of IL-17A suppression of IFN-γ. Neutrophil-depletion experiments, which dramatically reduce lung injury, revealed that neutrophils are primarily responsible for the IL-17A-dependent release of IL-33 into the airways. Taken together, our results reveal an IL-17A-neutrophil-axis that can drive IL-33 during helminth infection, highlighting an additional pathway by which IL-17A regulates pulmonary type 2 immunity.
Original language | English |
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Pages (from-to) | 767-775 |
Number of pages | 9 |
Journal | Mucosal Immunology |
Volume | 16 |
Issue number | 6 |
Early online date | 30 Sept 2023 |
DOIs | |
Publication status | Published - Dec 2023 |
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Dive into the research topics of 'The IL-17A-neutrophil axis promotes epithelial cell IL-33 production during nematode lung migration'. Together they form a unique fingerprint.Projects
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Molecular Regulators of the Alarmin IL-33 in Health and Disease
McSorley, H. (Investigator)
1/07/21 → 30/06/26
Project: Research