| First Author | Kwong B | Year | 2017 |
| Journal | Nat Immunol | Volume | 18 |
| Issue | 10 | Pages | 1117-1127 |
| PubMed ID | 28805812 | Mgi Jnum | J:260267 |
| Mgi Id | MGI:6140308 | Doi | 10.1038/ni.3816 |
| Citation | Kwong B, et al. (2017) T-bet-dependent NKp46(+) innate lymphoid cells regulate the onset of TH17-induced neuroinflammation. Nat Immunol 18(10):1117-1127 |
| abstractText | The transcription factor T-bet has been associated with increased susceptibility to systemic and organ-specific autoimmunity, but the mechanism by which T-bet expression promotes neuroinflammation remains unknown. In this study, we demonstrate a cardinal role of T-bet-dependent NKp46(+) innate lymphoid cells (ILCs) in the initiation of CD4(+) TH17-mediated neuroinflammation. Loss of T-bet specifically in NKp46(+) ILCs profoundly impaired the ability of myelin-reactive TH17 cells to invade central nervous system (CNS) tissue and protected the mice from autoimmunity. T-bet-dependent NKp46(+) ILCs localized in the meninges and acted as chief coordinators of meningeal inflammation by inducing the expression of proinflammatory cytokines, chemokines and matrix metalloproteinases, which together facilitated T cell entry into CNS parenchyma. Our findings uncover a detrimental role of T-bet-dependent NKp46(+) ILCs in the development of CNS autoimmune disease. |
