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Related Experiment Video

Updated: May 14, 2026

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

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

Published on: June 20, 2025

Interleukin-17 in post-stroke neurodegeneration.

Walter Swardfager¹, Daniel A Winer, Nathan Herrmann

¹Neuropsychopharmacology Research Group, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario M4N 3M5, Canada.

Neuroscience and Biobehavioral Reviews

|February 2, 2013

Summary

Interleukin-17 (IL-17) producing T lymphocytes worsen stroke outcomes by driving inflammation and cell death. Targeting IL-17 pathways may improve recovery and prevent long-term disability after stroke.

Related Experiment Videos

Last Updated: May 14, 2026

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

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

Published on: June 20, 2025

Area of Science:

Neuroscience
Immunology
Pathology

Background:

Stroke is a primary cause of disability, leading to neurodegeneration like dementia and depression.
Inflammation, particularly apoptotic cell death in ischemic tissue, significantly impacts stroke severity.
T lymphocytes infiltrating the brain post-stroke play a critical role in modulating inflammatory responses.

Purpose of the Study:

To review the role of Interleukin-17 (IL-17) secreting cells in post-stroke brain pathology.
To highlight potential therapeutic targets within the IL-17 axis for stroke recovery.

Main Methods:

Review of existing animal models and human studies on T lymphocytes and inflammatory mediators post-stroke.
Analysis of the involvement of IL-17 and its related cytokines (IL-23, IL-21) in stroke-induced tissue damage.
Examination of interactions between the IL-17 axis, innate immunity, and regulatory pathways.

Main Results:

T lymphocytes, including CD4(+) αβ and CD4(-) γδ T cells, are implicated as key mediators of brain damage post-stroke via IL-17 production.
The IL-17 axis contributes to tissue damage during the delayed inflammatory phase following ischemic events.
Positive feedback mechanisms amplify IL-17 signaling, prolonging or intensifying inflammatory responses.

Conclusions:

IL-17 secreting T lymphocytes are significant contributors to post-stroke brain pathology.
Targeting IL-17 pathways offers potential therapeutic strategies to mitigate inflammation, enhance recovery, and prevent long-term neurological decline.
Intervention in IL-17 regulatory pathways may improve patient outcomes and quality of life after stroke.