A class of immune cells has been implicated that have a harmful role in the late phase of ischemic brain injury, according to a study in this week's Nature Medicine.
Immune cell recruitment and activation have been implicated in the progression of brain damage after stroke, but the relevant cell populations had remained unknown.
Akihiko Yoshimura and colleagues focused on an immune cell population known as gamma-delta-T, which initiates the production of interleukin-17 (IL-17) an immune system signaling cell. They found that the infiltration of gamma-delta-T cells into the brain of mice, and the production of IL-17 by these cells, have a deleterious role on brain cells after a stroke.
Interestingly, the levels IL-17 peaked three days after stroke, pointing to a role for this cytokine in the late phase of brain injury. Moreover, keeping gamma-delta-T cells from entering the nervous system ameliorated the brain injury symptoms after stroke.
The authors propose that gamma-delta-T cells could be a therapeutic target against the inflammatory events that worsen the initial damage after a stroke.