| First Author | Huang H | Year | 2026 |
| Journal | Immunity | PubMed ID | 42561936 |
| Mgi Jnum | J:391198 | Mgi Id | MGI:8400288 |
| Doi | 10.1016/j.immuni.2026.07.011 | Citation | Huang H, et al. (2026) Group 2 innate lymphoid cells activate myelin-reactive T cells to augment neuroinflammation. Immunity |
| abstractText | The meninges are a gateway for pathogenic T cells to enter the central nervous system (CNS). They possess a diverse repertoire of immune cells that orchestrate CNS inflammation and autoimmunity, yet the underlying mechanisms are poorly understood. Here, we report that group 2 innate lymphoid cells (ILC2s) accumulated in the dura as experimental autoimmune encephalomyelitis (EAE) progressed. Single-cell RNA sequencing and flow cytometry analyses revealed distinct features of ILC2s, including expression of MHC class II. ILC2s acted as antigen-presenting cells to activate and expand myelin-reactive T cells in an MHC class II-dependent manner. ILC2-mediated expansion of myelin-reactive T cells increased expression of cytokines IFN-gamma and IL-17A. Genetic ablation of ILC2s or of H2-Ab1 in ILC2s alleviated neuroinflammation and CNS demyelination during EAE. These findings revealed a role of ILC2s in neuroinflammation via instructing myelin-reactive T cells, implying targeting ILC2s may be an avenue to restrict CNS inflammation and autoimmunity. |
