Abstract:

The evolution of ischemic brain damage is dramatically affected by the immune system, whose activation occurs immediately after the insult and may last for several days, involving a complex interplay between soluble and cellular mediators. Accordingly, recent expression profiling studies have revealed that the majority of the genes modulated in the blood of stroke patients participate to the regulation of innate immune responses. Moreover, in the clinical setting, serum levels of markers of acute inflammation correlate with the severity of ischemic brain damage and neurological deficit. Brain resident microglia and blood-borne immune cells crucially contribute to the acute and chronic processes implicated in tissue injury, as well as to the regenerative and reparative mechanisms that limit the damage and provide tissue healing and recovery. In this context, an attractive approach to improve successful clinical translation of stroke therapeutics would consist in achieving a rational modulation of the immune system, by blocking its detrimental inflammatory responses while promoting its beneficial components. This perspective commentary will focus on the most recent findings regarding relevant targets and drugs for immunomodulation in stroke and their potential application in patients.