T cells modulate the microglial response to brain ischemia.

Area of Science:

• Neuroimmunology
• Stroke Pathophysiology

Background:

• Neuroinflammation is critical post-stroke, involving microglia and leukocyte infiltration.
• Lymphocytes, despite low numbers, significantly contribute to secondary brain injury after stroke.

Purpose of the Study:

• To elucidate the mechanism by which lymphocytes influence stroke outcome.
• To investigate T cell modulation of microglial activation and its impact on stroke pathology.

Main Methods:

• Utilized a mouse model of ischemic stroke.
• Analyzed microglial gene expression in response to distinct T cell subpopulations (T_H1, T_REG).
• Assessed the effect of engineered T cells overexpressing IL-10 on microglial phenotype and infarct volume.

Main Results:

• T_H1 cells induced type I interferon signaling in microglia; T_REG cells promoted chemotaxis-associated genes.
• Engineered T cells shifted microglial gene expression towards pro-regenerative profiles.
• T cell-mediated microglia polarization did not alter acute infarct volume but influenced microglial phenotype.

Conclusions:

• T cells play a crucial role in stroke by polarizing microglial phenotypes.
• Targeting T cell-microglia interactions presents a viable strategy for stroke and neuroinflammation therapies.