| First Author | Yoshimura S | Year | 2020 |
| Journal | J Immunol | Volume | 204 |
| Issue | 3 | Pages | 531-539 |
| PubMed ID | 31852750 | Mgi Jnum | J:284037 |
| Mgi Id | MGI:6388991 | Doi | 10.4049/jimmunol.1801113 |
| Citation | Yoshimura S, et al. (2020) IL-9 Controls Central Nervous System Autoimmunity by Suppressing GM-CSF Production. J Immunol 204(3):531-539 |
| abstractText | Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) are inflammatory diseases of the CNS in which Th17 cells play a major role in the disease pathogenesis. Th17 cells that secrete GM-CSF are pathogenic and drive inflammation of the CNS. IL-9 is a cytokine with pleiotropic functions, and it has been suggested that it controls the pathogenic inflammation mediated by Th17 cells, and IL-9R(-/-) mice develop more severe EAE compared with wild-type counterparts. However, the underlying mechanism by which IL-9 suppresses EAE has not been clearly defined. In this study, we investigated how IL-9 modulates EAE development. By using mice knockout for IL-9R, we show that more severe EAE in IL-9R(-/-) mice correlates with increased numbers of GM-CSF(+) CD4(+) T cells and inflammatory dendritic cells (DCs) in the CNS. Furthermore, DCs from IL-9R(-/-) mice induced more GM-CSF production by T cells and exacerbated EAE upon adoptive transfer than did wild-type DCs. Our results suggest that IL-9 reduces autoimmune neuroinflammation by suppressing GM-CSF production by CD4(+) T cells through the modulation of DCs. |
