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Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
Published on: February 12, 2016
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Brain-infiltrating ILC2s boost poststroke angiogenic initiation through α-CGRP production.
An Ping1,2,3, Fan Yang1,2, Lingxiao Lu1,2
1Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
The Journal of Experimental Medicine
|August 25, 2025
Summary
Group 2 innate lymphoid cells (ILC2s) infiltrate the brain after ischemic stroke. These cells promote recovery by initiating blood vessel growth via alpha-calcitonin gene-related peptide (α-CGRP).
Area of Science:
- Neuroscience
- Immunology
- Vascular Biology
Background:
- Group 2 innate lymphoid cells (ILC2s) are crucial for tissue repair but scarce in the brain.
- Their infiltration mechanisms and role in brain repair, particularly after stroke, are largely unknown.
- ILC2s are recognized for immunosuppression in neuroinflammation, but their regenerative potential is underexplored.
Purpose of the Study:
- To investigate if ILC2s can enter the brain post-stroke and their functional role in recovery.
- To elucidate the mechanisms by which ILC2s influence brain tissue repair.
- To explore the therapeutic potential of ILC2s in stroke recovery.
Main Methods:
- In vivo and in vitro expansion of ILC2s.
- Tracking ILC2 brain infiltration in a mouse model of ischemic stroke.
- Assessing sensory-motor function recovery and angiogenesis initiation.
- Investigating the role of CXCR1, α-calcitonin gene-related peptide (α-CGRP), and CGRP receptors.
Main Results:
- ILC2s infiltrate the brain parenchyma from the bloodstream early after ischemic stroke in a CXCR1-dependent manner.
- Brain-infiltrating ILC2s enhance long-term sensory-motor recovery by promoting angiogenic sprouting.
- ILC2s produce α-CGRP, which is essential for initiating angiogenesis, acting on CGRP receptors on cerebrovascular endothelial cells.
Conclusions:
- ILC2s can infiltrate the brain after ischemic stroke and promote functional recovery.
- The mechanism involves ILC2-derived α-CGRP-mediated enhancement of angiogenic sprouting.
- ILC2s represent a promising therapeutic target for promoting angiogenesis and recovery post-stroke.
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