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

Research output: Contribution to journalJournal article

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  • Lucy H Jackson-Jones
  • Dominik Rückerl
  • Freya Svedberg
  • Sheelagh Duncan
  • Rick M Maizels
  • Tara E Sutherland
  • Stephen J Jenkins
  • Henry J McSorley
  • Cécile Bénézech
  • Andrew S MacDonald
  • Judith E Allen
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<mark>Journal publication date</mark>10/2016
<mark>Journal</mark>European Journal of Immunology
Issue number10
Volume46
Number of pages11
Pages (from-to)2311-2321
Publication StatusPublished
Early online date11/10/16
<mark>Original language</mark>English

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.