Group-2 innate lymphoid cell-dependent regulation of tissue neutrophil migration by alternatively activated macrophage-secreted Ear11
Jolin, Helen E.
Heycock, Morgan W. D.
Walker, Jennifer A.
Rana, Batika M. J.
Drynan, Lesley F.
Easton, Andrew J.
Oedekoven, Caroline A.
Kent, David G.
Fallon, Padraic G.
Barlow, Jillian L.
Nature Publishing Group US
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Panova, V., Gogoi, M., Rodriguez-Rodriguez, N., Sivasubramaniam, M., Jolin, H. E., Heycock, M. W. D., Walker, J. A., et al. (2020). Group-2 innate lymphoid cell-dependent regulation of tissue neutrophil migration by alternatively activated macrophage-secreted Ear11. Mucosal Immunology, 14 (1), 26-37. https://doi.org/10.1038/s41385-020-0298-2
Abstract: Type-2 immunity is characterised by interleukin (IL)-4, IL-5 and IL-13, eosinophilia, mucus production, IgE, and alternatively activated macrophages (AAM). However, despite the lack of neutrophil chemoattractants such as CXCL1, neutrophils, a feature of type-1 immunity, are observed in type-2 responses. Consequently, alternative mechanisms must exist to ensure that neutrophils can contribute to type-2 immune reactions without escalation of deleterious inflammation. We now demonstrate that type-2 immune-associated neutrophil infiltration is regulated by the mouse RNase A homologue, eosinophil-associated ribonuclease 11 (Ear11), which is secreted by AAM downstream of IL-25-stimulated ILC2. Transgenic overexpression of Ear11 resulted in tissue neutrophilia, whereas Ear11-deficient mice have fewer resting tissue neutrophils, whilst other type-2 immune responses are not impaired. Notably, administration of recombinant mouse Ear11 increases neutrophil motility and recruitment. Thus, Ear11 helps maintain tissue neutrophils at homoeostasis and during type-2 reactions when chemokine-producing classically activated macrophages are infrequently elicited.
External DOI: https://doi.org/10.1038/s41385-020-0298-2
This record's URL: https://www.repository.cam.ac.uk/handle/1810/315832
Attribution 4.0 International (CC BY 4.0)
Licence URL: https://creativecommons.org/licenses/by/4.0/