The mechanisms of neurorepair after stroke!
Stroke is a leading cause of adult disability but the mechanisms that support neurogenesis and neurorepair post-stroke is not clearly understood.
The researchers report that group 2 innate lymphoid cells (ILC2s) accumulate within the lesion core and subventricular zone (SVZ) during brain recovery following cerebral ischemia and facilitate neurorepair by producing Areg to expand NSPCs.
Mice with ILC2 deficiency display impaired neurological scoring post-stroke and transfer of ILC2s or administration of Areg markedly improves neurological outcomes post-stroke.
These findings suggest that ILC2s and their products may provide promising therapeutic opportunities for neurorepair following brain injury.
