Deans' stroke musings: ILC2 instructs neural stem and progenitor cells to potentiate neurorepair after stroke

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, April 16, 2025

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

Do you really think your incompetent doctor and hospital can get human testing going and create protocols on this? If they don't, they just completely proved their incompetence! Why hasn't the board of directors been fired yet?

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

Gaoyu Liu^1,2,3,6 ∙ Huachen Huang^4,6 ∙ Ying Wang^2,6 ∙ … ∙ Ying Yu⁵ yuying@tmu.edu.cn ∙ Qiang Liu⁴ qliu@tmu.edu.cn ∙ Jie Zhou^1,2,7 zhoujie@tmu.edu.cn … Show more

Highlights

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Brain-infiltrated ILC2 attenuates neurological deficits post-stroke

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ILC2s within the brain display unique immune profiles from those in the periphery

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ILC2s promote neurogenesis and neuronal recovery post-stroke

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ILC2-derived Areg expands neural progenitors in the SVZ post-stroke

Summary

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.