Suppressing Immunosuppression after Stroke

There is growing evidence that acute injury of the central nervous system, including stroke, impairs the immune system. A recent study implicates the postischemic activation of a particular type of lymphocyte, by noradrenergic signaling, as a mediator of impairment. Pneumonia is a major cause of death after acute cerebral ischemia. A recent study by Wong and colleagues 1 provides some insight into susceptibility to infection after stroke. Specifically, they found that infections after stroke are promoted by noradrenergic-mediated dysfunction of a small subset of lymphocytes — the invariant natural killer T cells. More than 40% of patients die within a few weeks after stroke or have severe long-term disabilities. Although two thirds of these outcomes are attributed to nonmodifiable factors, such as the severity of the initial stroke and the patient's age, the remaining third is consequent to modifiable factors . . .