The best approach to stroke is to prevent it from happening, a goal that implies a robust way to control and reverse atherosclerosis, the development of fatty lesions that narrow and weaken blood vessels. There is still only limited progress towards more meaningful treatments for atherosclerosis, unfortunately, and so the research community remains very interested in finding ways to limit the damage that occurs following a stroke, or enhance regeneration of damaged brain tissue. The immune system plays an important role in the post-stroke environment, and researchers here report on an interesting discovery, a population of immune cells that appears important in limiting the damage of stroke in the days following the event.
Immune response plays an important role in stroke. As soon as a blood clot wedges itself in a blood vessel, the brain sends an "SOS" signal to activate the immune system. This rapid immune response aims to clear out the cell debris, limit brain damage, and kick-start brain repair processes. However, the function of the immune system is diverse and complex, and different types of immune cells may play distinct beneficial or detrimental roles in a damaged brain.
This study identified a novel subset of CD8+ regulatory-like T cells, or CD8+TRLs, as "first responders" to stroke. Attracted to the site of ischemic injury by a unique "homing" signal released by dying brain cells, CD8+TRLs reach the brain within 24 hours after stroke onset, where they release molecules that provide direct neuroprotective effects, as well as limit inflammation and secondary brain damage. "Creating shelf-stable and ready-to-use CD8+TRLs or developing a cocktail of neuroprotective signaling molecules released by those cells once they reach the brain could present effective future therapies against stroke and offer hope to hundreds of thousands of patients who are ineligible for treatments available to them currently."
CD8+TRLs enter the brain much faster than any other regulatory immune cells. Within 24 hours after researchers depleted these special CD8+TRLs from the bloodstream of stroke mice, the size of the brain region affected by ischemia expanded by 50% compared to animals whose CD8+TRL levels remained intact. Even more reassuringly, mice who received a transfusion of purified CD8+TRLs prepared in the lab fared better and recovered faster than those who were untreated for over five weeks. These unique CD8+TRLs, therefore, serve as early responders to rally defenses after stroke and may collaborate with other immune cells to safeguard the brain for a long time.