| First Author | Fu Y | Year | 2022 |
| Journal | Sci Immunol | Volume | 7 |
| Issue | 68 | Pages | eabi9768 |
| PubMed ID | 35179949 | Mgi Jnum | J:360399 |
| Mgi Id | MGI:7797511 | Doi | 10.1126/sciimmunol.abi9768 |
| Citation | Fu Y, et al. (2022) An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment. Sci Immunol 7(68):eabi9768 |
| abstractText | Despite IL-9 functioning as a pleiotropic cytokine in mucosal environments, the IL-9-responsive cell repertoire is still not well defined. Here, we found that IL-9 mediates proallergic activities in the lungs by targeting lung macrophages. IL-9 inhibits alveolar macrophage expansion and promotes recruitment of monocytes that develop into CD11c(+) and CD11c(-) interstitial macrophage populations. Interstitial macrophages were required for IL-9-dependent allergic responses. Mechanistically, IL-9 affected the function of lung macrophages by inducing Arg1 activity. Compared with Arg1-deficient lung macrophages, Arg1-expressing macrophages expressed greater amounts of CCL5. Adoptive transfer of Arg1(+) lung macrophages but not Arg1(-) lung macrophages promoted allergic inflammation that Il9r(-/-) mice were protected against. In parallel, the elevated expression of IL-9, IL-9R, Arg1, and CCL5 was correlated with disease in patients with asthma. Thus, our study uncovers an IL-9/macrophage/Arg1 axis as a potential therapeutic target for allergic airway inflammation. |
