HEAD-INJURY - AN IMMUNOLOGICAL DEFICIT IN T-CELL ACTIVATION

Despite progress in the management of increased pressure following head injury, infection remains the most common complication in survivors. This study attempted to better define the immunologic deficit that occurs immediately and in the early post-recovery period following severe head injury. Twenty-seven patients admitted with the primary diagnosis of severe head injury (mean Glasgow Coma Score, 6.75) were studied within 24 hours of injury and at weekly intervals. T-cell proliferative response to mitogen stimulation was assessed. T-cell antigen expression following PHA stimulation was assessed for helper (CD4) and suppressor (CD8) subpopulations: the early T-cell activation antigens interleukin-2 receptor (IL2R) and transferrin receptor (TFR), and the late antigen (HLA-DR) using flow cytometry. Polymorphonuclear leukocyte function was assessed using oxidative burst. There was a reduction in the proliferative response of T cells to mitogen stimulation. The B-cell response seemed unaffected. The diminished proliferative response was accompanied by diminished expression of early activation antigens (IL2R and TFR) and late (following DNA synthesis) (HLA- DR). This was seen primarily on helper/inducer cells (CD4+). Polymorphonuclear leukocyte function was unaffected. © 1990 by The Williams and Wilkins Co.