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IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha

IL‐33 plays an important role in the initiation of type‐2 immune responses, as well as the enhancement of type 2 effector functions. Engagement of the IL‐33 receptor on macrophages facilitates polarization to an alternative activation state by amplifying IL‐4 and IL‐13 signaling to IL‐4Rα. IL‐4 and...

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Autores principales: Jackson‐Jones, Lucy H., Rückerl, Dominik, Svedberg, Freya, Duncan, Sheelagh, Maizels, Rick M., Sutherland, Tara E., Jenkins, Stephen J., McSorley, Henry J., Bénézech, Cécile, MacDonald, Andrew S., Allen, Judith E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082546/
https://www.ncbi.nlm.nih.gov/pubmed/27592711
http://dx.doi.org/10.1002/eji.201646442
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author Jackson‐Jones, Lucy H.
Rückerl, Dominik
Svedberg, Freya
Duncan, Sheelagh
Maizels, Rick M.
Sutherland, Tara E.
Jenkins, Stephen J.
McSorley, Henry J.
Bénézech, Cécile
MacDonald, Andrew S.
Allen, Judith E.
author_facet Jackson‐Jones, Lucy H.
Rückerl, Dominik
Svedberg, Freya
Duncan, Sheelagh
Maizels, Rick M.
Sutherland, Tara E.
Jenkins, Stephen J.
McSorley, Henry J.
Bénézech, Cécile
MacDonald, Andrew S.
Allen, Judith E.
author_sort Jackson‐Jones, Lucy H.
collection PubMed
description IL‐33 plays an important role in the initiation of type‐2 immune responses, as well as the enhancement of type 2 effector functions. Engagement of the IL‐33 receptor on macrophages facilitates polarization to an alternative activation state by amplifying IL‐4 and IL‐13 signaling to IL‐4Rα. IL‐4 and IL‐13 also induce macrophage proliferation but IL‐33 involvement in this process has not been rigorously evaluated. As expected, in vivo delivery of IL‐33 induced IL‐4Rα‐dependent alternative macrophage activation in the serous cavities. IL‐33 delivery also induced macrophages to proliferate but, unexpectedly, this was independent of IL‐4Rα signaling. In a filarial nematode infection model in which IL‐4Rα‐dependent alternative activation and proliferation in the pleural cavity is well described, IL‐33R was essential for alternative activation but not macrophage proliferation. Similarly, during Alternaria alternata induced airway inflammation, which provokes strong IL‐33 responses, we observed that both IL‐4Rα and IL‐33R were required for alternative activation, while macrophage proliferation in the pleural cavity was still evident in the absence of either receptor alone. Our data show that IL‐33R and IL‐4Rα promote macrophage proliferation independently of each other, but both are essential for induction of alternative activation.
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spelling pubmed-50825462016-11-09 IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha Jackson‐Jones, Lucy H. Rückerl, Dominik Svedberg, Freya Duncan, Sheelagh Maizels, Rick M. Sutherland, Tara E. Jenkins, Stephen J. McSorley, Henry J. Bénézech, Cécile MacDonald, Andrew S. Allen, Judith E. Eur J Immunol Innate immunity IL‐33 plays an important role in the initiation of type‐2 immune responses, as well as the enhancement of type 2 effector functions. Engagement of the IL‐33 receptor on macrophages facilitates polarization to an alternative activation state by amplifying IL‐4 and IL‐13 signaling to IL‐4Rα. IL‐4 and IL‐13 also induce macrophage proliferation but IL‐33 involvement in this process has not been rigorously evaluated. As expected, in vivo delivery of IL‐33 induced IL‐4Rα‐dependent alternative macrophage activation in the serous cavities. IL‐33 delivery also induced macrophages to proliferate but, unexpectedly, this was independent of IL‐4Rα signaling. In a filarial nematode infection model in which IL‐4Rα‐dependent alternative activation and proliferation in the pleural cavity is well described, IL‐33R was essential for alternative activation but not macrophage proliferation. Similarly, during Alternaria alternata induced airway inflammation, which provokes strong IL‐33 responses, we observed that both IL‐4Rα and IL‐33R were required for alternative activation, while macrophage proliferation in the pleural cavity was still evident in the absence of either receptor alone. Our data show that IL‐33R and IL‐4Rα promote macrophage proliferation independently of each other, but both are essential for induction of alternative activation. John Wiley and Sons Inc. 2016-10-11 2016-10 /pmc/articles/PMC5082546/ /pubmed/27592711 http://dx.doi.org/10.1002/eji.201646442 Text en © 2016 The Authors. European Journal of Immunology published by WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Innate immunity
Jackson‐Jones, Lucy H.
Rückerl, Dominik
Svedberg, Freya
Duncan, Sheelagh
Maizels, Rick M.
Sutherland, Tara E.
Jenkins, Stephen J.
McSorley, Henry J.
Bénézech, Cécile
MacDonald, Andrew S.
Allen, Judith E.
IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha
title IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha
title_full IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha
title_fullStr IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha
title_full_unstemmed IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha
title_short IL‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha
title_sort il‐33 delivery induces serous cavity macrophage proliferation independent of interleukin‐4 receptor alpha
topic Innate immunity
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082546/
https://www.ncbi.nlm.nih.gov/pubmed/27592711
http://dx.doi.org/10.1002/eji.201646442
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