Jackson-Jones, Lucy H and Rückerl, Dominik and Svedberg, Freya and Duncan, Sheelagh and Maizels, Rick M and Sutherland, Tara E and Jenkins, Stephen J and McSorley, Henry J and Bénézech, Cécile and MacDonald, Andrew S and Allen, Judith E (2016) IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha. European Journal of Immunology, 46 (10). pp. 2311-2321. ISSN 0014-2980
Full text not available from this repository.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.