Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Therapeutic Potential of Group 2 Innate Lymphoid Cells in Neuroinflammatory Diseases.

Scandinavian journal of immunology·2026
Same author

Blood-brain barrier breakdown in traumatic brain injury: current insights and future directions.

Cancer gene therapy·2026
Same author

Cortical representation of multidimensional handwriting movement and implications for neuroprostheses.

Nature communications·2026
Same author

Repopulating Microglia Suppress Peripheral Immune Cell Infiltration to Promote Poststroke Recovery.

CNS neuroscience & therapeutics·2025
Same author

Plasmablast-like lymphoma cells as a distinct subpopulation confer multidrug resistance in PCNSL.

Neuro-oncology·2025
Same author

Construction of a Prognostic Model Using RNA Processing Factor Genes and the Key Role of NSUN6 in Glioma Outcomes.

Journal of cellular and molecular medicine·2025

Related Experiment Video

Updated: May 8, 2026

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
12:14

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

35.2K

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
PubMed
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).

More Related Videos

Injection of Hydrogel Biomaterial Scaffolds to The Brain After Stroke
09:41

Injection of Hydrogel Biomaterial Scaffolds to The Brain After Stroke

Published on: October 1, 2020

5.3K
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
08:23

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

147

Related Experiment Videos

Last Updated: May 8, 2026

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
12:14

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

35.2K
Injection of Hydrogel Biomaterial Scaffolds to The Brain After Stroke
09:41

Injection of Hydrogel Biomaterial Scaffolds to The Brain After Stroke

Published on: October 1, 2020

5.3K
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
08:23

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

147

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.