Modulation of the Post-Ischemic Immune Response Improves Outcome in Focal Cerebral Ischemia: A Role for Lymphocytes in Stroke?

Inflammation appears to contribute to ischemic brain injury [5 16]. The factors that incite the inflammatory response are not clear, but break down of the blood-brain barrier (BBB) exposes the brain to the peripheral circulation and thus the systemic immune system. Following stroke, antigens found either primarily or exclusively in the central nervous system (CNS), like neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), S-100 protein, and creatine phosphokinase (CPK)-BB, can be found within the plasma [8 13 14 43 57]. Furthermore, the plasma levels of these antigens correlate to eventual infarct size and neurological outcome [8 13 14 43 57]. This systemic encounter with CNS antigens may explain why there is an increase in the number of circulating lymphocytes and immunoglobulins that react with CNS antigens following stroke [1 28 60].