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

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IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha. / Jackson-Jones, Lucy H; Rückerl, Dominik; Svedberg, Freya et al.
In: European Journal of Immunology, Vol. 46, No. 10, 10.2016, p. 2311-2321.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Jackson-Jones, LH, Rückerl, D, Svedberg, F, Duncan, S, Maizels, RM, Sutherland, TE, Jenkins, SJ, McSorley, HJ, Bénézech, C, MacDonald, AS & Allen, JE 2016, 'IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha', European Journal of Immunology, vol. 46, no. 10, pp. 2311-2321. https://doi.org/10.1002/eji.201646442

APA

Jackson-Jones, L. H., Rückerl, D., Svedberg, F., Duncan, S., Maizels, R. M., Sutherland, T. E., Jenkins, S. J., McSorley, H. J., Bénézech, C., MacDonald, A. S., & Allen, J. E. (2016). IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha. European Journal of Immunology, 46(10), 2311-2321. https://doi.org/10.1002/eji.201646442

Vancouver

Jackson-Jones LH, Rückerl D, Svedberg F, Duncan S, Maizels RM, Sutherland TE et al. IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha. European Journal of Immunology. 2016 Oct;46(10):2311-2321. Epub 2016 Oct 11. doi: 10.1002/eji.201646442

Author

Jackson-Jones, Lucy H ; Rückerl, Dominik ; Svedberg, Freya et al. / IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha. In: European Journal of Immunology. 2016 ; Vol. 46, No. 10. pp. 2311-2321.

Bibtex

@article{54b395ebc12245aabf636a247f8b9de1,
title = "IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha",
abstract = "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.",
keywords = "Alternaria, Alternariosis, Animals, Cell Proliferation, Cells, Cultured, Filariasis, Filarioidea, Interleukin-1 Receptor-Like 1 Protein, Interleukin-33, Macrophage Activation, Macrophages, Mice, Mice, Inbred BALB C, Mice, Knockout, Pleural Cavity, Receptors, Cell Surface, Serous Membrane, Signal Transduction, Journal Article, Research Support, Non-U.S. Gov't",
author = "Jackson-Jones, {Lucy H} and Dominik R{\"u}ckerl and Freya Svedberg and Sheelagh Duncan and Maizels, {Rick M} and Sutherland, {Tara E} and Jenkins, {Stephen J} and McSorley, {Henry J} and C{\'e}cile B{\'e}n{\'e}zech and MacDonald, {Andrew S} and Allen, {Judith E}",
note = "{\textcopyright} 2016 The Authors. European Journal of Immunology published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.",
year = "2016",
month = oct,
doi = "10.1002/eji.201646442",
language = "English",
volume = "46",
pages = "2311--2321",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley-VCH Verlag",
number = "10",

}

RIS

TY - JOUR

T1 - IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha

AU - Jackson-Jones, Lucy H

AU - Rückerl, Dominik

AU - Svedberg, Freya

AU - Duncan, Sheelagh

AU - Maizels, Rick M

AU - Sutherland, Tara E

AU - Jenkins, Stephen J

AU - McSorley, Henry J

AU - Bénézech, Cécile

AU - MacDonald, Andrew S

AU - Allen, Judith E

N1 - © 2016 The Authors. European Journal of Immunology published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

PY - 2016/10

Y1 - 2016/10

N2 - 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.

AB - 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.

KW - Alternaria

KW - Alternariosis

KW - Animals

KW - Cell Proliferation

KW - Cells, Cultured

KW - Filariasis

KW - Filarioidea

KW - Interleukin-1 Receptor-Like 1 Protein

KW - Interleukin-33

KW - Macrophage Activation

KW - Macrophages

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Knockout

KW - Pleural Cavity

KW - Receptors, Cell Surface

KW - Serous Membrane

KW - Signal Transduction

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1002/eji.201646442

DO - 10.1002/eji.201646442

M3 - Journal article

C2 - 27592711

VL - 46

SP - 2311

EP - 2321

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 10

ER -