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Updated: May 28, 2026
Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
Published on: February 12, 2016
Myelin specific cells infiltrate MCAO lesions and exacerbate stroke severity
Xuefang Ren1, Kozaburo Akiyoshi, Marjorie R Grafe
1Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA.
Abstract:
Although inflammatory responses increase stroke severity, the role of immune cells specific for central nervous system (CNS) antigens remains controversial. Disruption of the blood-brain barrier (BBB) during stroke allows CNS antigens to leak into the peripheral circulation and enhances access of circulating leukocytes to the brain, including those specific for CNS antigens such as myelin oligodendrocyte glycoprotein (MOG) that can induce experimental autoimmune encephalomyelitis (EAE). We here demonstrate for the first time that myelin reactive splenocytes specific for MOG transferred into severe combined immunodeficient (SCID) mice can migrate into the infarct hemisphere of recipients subjected to 60 min middle cerebral artery occlusion (MCAO) and 96 h reperfusion; moreover these cells exacerbate infarct volume and worsen neurological deficits compared to animals transferred with naïve splenocytes. These findings indicate that autoimmunity in the CNS can exert detrimental injury on brain cells and worsen the damage from ischemic stroke.
Insights
Immune cells targeting central nervous system (CNS) antigens worsen stroke damage. Myelin-reactive T cells exacerbated infarct volume and neurological deficits in mice after ischemic stroke.
Area of Science:
- Neuroimmunology
- Stroke research
- Autoimmunity
Background:
- Inflammatory responses exacerbate stroke severity.
- The role of CNS-antigen-specific immune cells in stroke is debated.
- Blood-brain barrier disruption during stroke allows immune cell infiltration.
Purpose of the Study:
- To investigate the impact of myelin-reactive T cells on ischemic stroke.
- To determine if CNS autoimmunity exacerbates stroke-induced brain damage.
Main Methods:
- Transfer of myelin oligodendrocyte glycoprotein (MOG)-reactive splenocytes into severe combined immunodeficient (SCID) mice.
- Induction of focal cerebral ischemia via middle cerebral artery occlusion (MCAO) in recipient mice.
- Assessment of infarct volume and neurological deficits 96 hours post-reperfusion.
Main Results:
- MOG-reactive splenocytes migrated to the infarct hemisphere in MCAO mice.
- Adoptive transfer of MOG-reactive cells significantly increased infarct volume.
- Mice receiving MOG-reactive cells exhibited worsened neurological deficits compared to controls.
Conclusions:
- CNS autoimmunity can be detrimental to brain cells during ischemic stroke.
- Myelin-reactive immune cells exacerbate ischemic brain injury and neurological deficits.
- These findings highlight a potential mechanism for autoimmune exacerbation of stroke damage.
