The Influence of Mechanical Trauma on the B-Cell System: Phenotypes, Terminal B-Cell Maturation, Immunoglobulin Synthesis and Influence of Lymphokines

Abstract

While many investigators agree that the trauma-induced breakdown of the lymphokine cascade (interleukins 1 and 2; IL-1, IL-2) is responsible for the lack of T-lymphocyte activation and proliferation following injury [7–9], its potential effect on B-cell responses has not been investigated extensively so far. While there have been some studies on specific and unspecific humoral immune responses in burned individuals [25, 30], there have been only a very limited number of observations made of humoral immune responses following major trauma. It is known that in patients who develop severe sepsis, the antibody-forming cell responses are profoundly depressed compared to those of patients who did not develop sepsis and who had normal amounts of antibody-forming cells [4]. Nohr et al. [20, 21] studied humoral immunity in surgical patients in vivo and in vitro. They found a deficiency of in vitro B-cell responses to tetanus toxoid compared to those of controls, who showed a population of B-cells that spontaneously secreted tetanus toxoid in vitro following immunization. In vitro antibody production in their study reflected the in vivo antibody responses. Nohr et al. concluded from their results that the failure of specific antibody production might be caused by a failure of the antigen recognition and/or lymphocyte activation in unresponsive surgical patients.