Stroke is one of the leading causes of death and disability worldwide. The limited utility of current treatments,
the increasing rates of stroke survivorship and subsequent long-term disability necessitate novel approaches to improve
functional recovery after injury. The underlying immune mechanisms mediating inflammation and subsequent repair
beyond the acute phase of injury remain understudied. The relative balance of injury and repair is dependent in part on the
polarization state of microglia, the resident tissue macrophage of the central nervous system. Microglia can be classically
activated to a pro-inflammatory phenotype, or alternatively activated to an immunomodulatory, tissue repair phenotype
depending on the balance of local environmental cues. Once activated, they orchestrate a complex symphony of
inflammation and repair, interacting with both the peripheral immune system and local cells such as astrocytes and neural
stem cells to coordinate the resolution of inflammation and repair of damaged tissues. Furthermore, neural stem cells and
astrocytes themselves appear to have intrinsic immunomodulatory properties which could be used in the development of
future therapies. Enhancing these “reparative” functions with pharmacologic agents could open up exciting new avenues
to improve long-term functional recovery in stroke patients.
Keywords: Inflammation, ischemia, microglia, recovery, stem cell, stroke, tissue repair.
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