| First Author | Ikutani M | Year | 2017 |
| Journal | JCI Insight | Volume | 2 |
| Issue | 7 | Pages | e90721 |
| PubMed ID | 28405615 | Mgi Jnum | J:290723 |
| Mgi Id | MGI:6443377 | Doi | 10.1172/jci.insight.90721 |
| Citation | Ikutani M, et al. (2017) Prolonged activation of IL-5-producing ILC2 causes pulmonary arterial hypertrophy. JCI Insight 2(7):e90721 |
| abstractText | IL-33 is one of the critical cytokines that activates group 2 innate lymphoid cells (ILC2s) and mediates allergic reactions. Accumulating evidence suggests that IL-33 is also involved in the pathogenesis of several chronic inflammatory diseases. Previously, we generated an IL-5 reporter mouse and revealed that lung IL-5-producing ILC2s played essential roles in regulating eosinophil biology. In this study, we evaluated the consequences of IL-33 administration over a long period, and we observed significant expansion of ILC2s and eosinophils surrounding pulmonary arteries. Unexpectedly, pulmonary arteries showed severe occlusive hypertrophy that was ameliorated in IL-5- or eosinophil-deficient mice, but not in Rag2-deficient mice. This indicates that IL-5-producing ILC2s and eosinophils play pivotal roles in pulmonary arterial hypertrophy. Administration of a clinically used vasodilator was effective in reducing IL-33-induced hypertrophy and repressed the expansion of ILC2s and eosinophils. Taken together, these observations demonstrate a previously unrecognized mechanism in the development of pulmonary arterial hypertrophy and the causative roles of ILC2 in the process. |
