Effect of brain injury on immunophenotype of peripheral blood lymphocytes in rats.

Strong immunosuppression occurs after severe traumatic brain injury (TBI) and most likely contributes substantially to the patient morbidity and mortality. However, the mechanisms of this immunosuppression are unknown. For the lowering of stressful factors, severe TBI was induced in anaesthetized rats. The lymphocyte subsets from 60 rats with severe TBI were analyzed using monoclonal antibody by the indirect immunofluorescence method. The blood of 30 rats without TBI was used as a control. When compared to the control group, the rats with TBI showed a remarkable reduction in the relative number of CD4(+), RT-Ia(+), Thy-1(+) and ICO-111(+) lymphocytes during the first 2 h after injury. Further reduction in the number of CD4(+) cells was determined in the rats during all the period of the experimental observation. The number of lymphocytes expressing membrane Thy-1 and ICO-111 antigens was significantly decreased 7 days after the trauma. The relative number of RT-Ia(+) lymphocytes was significantly reduced in rats with TBI during 14 days following the trauma. A significant decrease in the luminescence intensity of all the analyzed antigen-positive cells was also observed in rats with TBI. Between the 7th and the 14th days after the trauma a positive correlation between the number of Thy-1(+) PBLs and the number of RT-Ia(+) lymphocytes was determined. Similar results on lymphocyte immunophenotype were seen in patients with TBI. Thus, the cellular immune response is identical in patients and in animals with TBI. Severe brain traumatic injury leads to a reduced expression of cell surface antigens and causes a decrease in the number of antigen-positive lymphocytes and in the intensity of their luminescence.

Immunophenotype of Peripheral Blood Lymphocytes in Patients with Burns.

Severe immunosuppression occurs after large thermal burns and probably contributes substantially to patient morbidity and mortality. The mechanism of immunosuppression is much unknown. T lymphocyte subsets from 45 severely patients with burns and 35 healthy donors were analyzed using monoclonal antibodies by indirect immunofluorescence method. Compared to healthy donors, patients with burns have shown a profound reduction in relative number of CD3(+) lymphocytes during the 24-h period following injury, which was accompanied by a decrease in CD4 but not CD8 subsets. Activated lymphocytes, while determined by the expression of CD25, CD26 and CD71, were insignificantly increased in patients with burns. The expression HLA DR was insignificantly decreased on peripheral blood lymphocytes from thermally injured patients. Additionally, the significant decrease of CD95 antigen expression was observed in all patients with burns. Also, significant decrease of the luminescence intensity in all analyzed antigens was observed in patients with burns. Numerous positive correlations between CD3(+), CD8(+), CD25(+), CD26(+) and CD71(+) cells were revealed, especially during the first week after thermal trauma. We conclude that the thermal injury produces a profound relative CD3(+) and CD4(+) cell lymphopenia with signs of moderate lymphocyte activation.