Gaoyu Liu, Huachen Huang, Ying Wang, Yali Han, Jianye Wang, Mengxuan Shi, Pan Zhou, Chun Chen, Ying Yu, Qiang Liu, Jie Zhou
{"title":"ILC2 instructs neural stem and progenitor cells to potentiate neurorepair after stroke.","authors":"Gaoyu Liu, Huachen Huang, Ying Wang, Yali Han, Jianye Wang, Mengxuan Shi, Pan Zhou, Chun Chen, Ying Yu, Qiang Liu, Jie Zhou","doi":"10.1016/j.neuron.2025.03.014","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":19313,"journal":{"name":"Neuron","volume":" ","pages":"1741-1757.e7"},"PeriodicalIF":14.7000,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuron","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.neuron.2025.03.014","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/14 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
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.
期刊介绍：
Established as a highly influential journal in neuroscience, Neuron is widely relied upon in the field. The editors adopt interdisciplinary strategies, integrating biophysical, cellular, developmental, and molecular approaches alongside a systems approach to sensory, motor, and higher-order cognitive functions. Serving as a premier intellectual forum, Neuron holds a prominent position in the entire neuroscience community.
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