ILC2 instructs neural stem and progenitor cells to potentiate neurorepair after stroke.

Stroke affects approximately 1 in 6 individuals globally and is the leading cause of adult disability, which is attributed to neuronal damage and neurological impairments. The mechanisms by which the brain tissue microenvironment supports neurogenesis and neurorepair post-stroke remain to be fully elucidated. In this study, we report that group 2 innate lymphoid cells (ILC2s) accumulate within the lesion core and subventricular zone (SVZ) during brain recovery following cerebral ischemia. Mice with ILC2 deficiency display impaired neurological scoring post-stroke. Mechanistic studies reveal that brain ILC2s enhance the proliferation of neural stem and progenitor cells (NSPCs) through the secretion of amphiregulin (Areg). Adoptive transfer of ILC2s or administration of Areg markedly improves neurological outcomes post-stroke. These findings demonstrate that ILC2s and their secreted products may represent a promising therapeutic strategy for enhancing neurorepair following brain injury.