Immune consequences of stroke and cerebral palsy in adults

The possibility that brain damage results in a sustained dysregulation of lymphocyte responsiveness to the lymphokine, interleukin-2 (IL-2), was investigated in individuals who had experienced a unilateral stroke in adulthood or who presented with spastic hemiparesis since childhood. Following verification of unilateral brain damage via neuromotor assessment, and determination of their health status, blood samples were obtained to evaluate a panel of immune measures. Soluble interleukin-2 receptor (sIL-2R) and lymphocyte proliferative and cytolytic responses in the subjects with stroke or cerebral palsy were compared to age- and gender-matched controls. In addition, lymphocyte populations were enumerated via flow cytometry, and lymphocyte cyclic AMP (cAMP) levels were determined. Circulating blood levels of sIL-2R were significantly elevated in all individuals that had experienced unilateral brain damage. Cytolytic activity also failed to be stimulated to the normal level by in vitro treatment of lymphocytes with IL-2. Further, lymphocytes from the stroke subjects proliferated significantly less after mitogen and IL-2 stimulation. These functional differences were not accounted for by an abnormal leukocyte profile, although phenotypic analyses revealed subtle differences in the natural killer cell subsets. Overall, the findings indicate that individuals with brain damage may not respond appropriately when immune activation is required. These immune differences appear to be a stable trait given that they were manifested after both perinatal and adult brain insult in otherwise healthy, independently living individuals.