| First Author | Grigg JB | Year | 2021 |
| Journal | Nature | Volume | 600 |
| Issue | 7890 | Pages | 707-712 |
| PubMed ID | 34853467 | Mgi Jnum | J:339261 |
| Mgi Id | MGI:7287965 | Doi | 10.1038/s41586-021-04136-4 |
| Citation | Grigg JB, et al. (2021) Antigen-presenting innate lymphoid cells orchestrate neuroinflammation. Nature 600(7890):707-712 |
| abstractText | Pro-inflammatory T cells in the central nervous system (CNS) are causally associated with multiple demyelinating and neurodegenerative diseases(1-6), but the pathways that control these responses remain unclear. Here we define a population of inflammatory group 3 innate lymphoid cells (ILC3s) that infiltrate the CNS in a mouse model of multiple sclerosis. These ILC3s are derived from the circulation, localize in proximity to infiltrating T cells in the CNS, function as antigen-presenting cells that restimulate myelin-specific T cells, and are increased in individuals with multiple sclerosis. Notably, antigen presentation by inflammatory ILC3s is required to promote T cell responses in the CNS and the development of multiple-sclerosis-like disease in mouse models. By contrast, conventional and tissue-resident ILC3s in the periphery do not appear to contribute to disease induction, but instead limit autoimmune T cell responses and prevent multiple-sclerosis-like disease when experimentally targeted to present myelin antigen. Collectively, our data define a population of inflammatory ILC3s that is essential for directly promoting T-cell-dependent neuroinflammation in the CNS and reveal the potential of harnessing peripheral tissue-resident ILC3s for the prevention of autoimmune disease. |
