| First Author | Jackson-Jones LH | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 10 | Pages | 2311-2321 |
| PubMed ID | 27592711 | Mgi Jnum | J:246485 |
| Mgi Id | MGI:5923500 | Doi | 10.1002/eji.201646442 |
| Citation | Jackson-Jones LH, et al. (2016) IL-33 delivery induces serous cavity macrophage proliferation independent of interleukin-4 receptor alpha. Eur J Immunol 46(10):2311-2321 |
| abstractText | 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-4Ralpha. 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-4Ralpha-dependent alternative macrophage activation in the serous cavities. IL-33 delivery also induced macrophages to proliferate but, unexpectedly, this was independent of IL-4Ralpha signaling. In a filarial nematode infection model in which IL-4Ralpha-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-4Ralpha 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-4Ralpha promote macrophage proliferation independently of each other, but both are essential for induction of alternative activation. |
