Markers for cell-mediated immune response are elevated in cerebrospinal fluid and serum after severe traumatic brain injury in humans

The brain is believed to be an immunologically privileged organ, sheltered from the systemic immunological defense by the blood-brain barrier (BBB). H owever, there is increasing evidence for a marked inflammatory response in the brain after traumatic brain injury (TBI), Markers for cellular immune a ctivation, neopterin, beta2-microglobulin (beta 2M), and soluble interleuki n-2 receptor (sIL-2R), were measured for up to 3 weeks in cerebrospinal flu id (CSF) and serum of 41 patients with severe TBI in order to elucidate the time course and the origin of the cellular immune response following TBI. Neopterin gradually increased during the first posttraumatic week in both C SF and serum. Concentrations in CSF were generally higher than in serum, su ggesting intrathecal release of this marker. beta 2M showed similar kinetic s but with higher serum than CSF concentrations. Nonetheless, intrathecal r elease as assessed by the beta 2M index could be postulated for most of the patients. The mean levels of sIL-2R in both CSF and serum were elevated du ring the whole study period, serum concentrations being up to 2 x 10(4) tim es higher than in CSF. No significant intrathecal production of sIL-2R coul d be detected. The present data shows that severe TBI leads to a marked cel l-mediated immune response within the brain and in the systemic circulation . In the intrathecal compartment the activated cells appear to be predomina ntly of the macrophage/microglia lineage, while the immune activation in th e systemic circulation seems to involve mainly T-lymphocytes.