SPECIFIC CHANGES IN LYMPHOCYTE SUBPOPULATIONS - A POTENTIAL MECHANISM FOR STRESS-INDUCED IMMUNOMODULATION

The mechanisms by which stressors alter immune function are not well understood. One hypothesis for stress-induced immunomodulation is that since immune responses require cooperation of different cell types, stress-induced shifts in cell populations might affect an organism's ability to mount an immune response. We sought to determine if inescapable shock (IS) could alter lymphocyte subpopulations and if so, whether this could be a mechanism for shock-induced immunomodulation. Our results suggest that IS produces changes in lymphocyte subpopulations and that these shifts could be responsible for modulation of in vivo antibody production. Exposure to IS resulted in an increase in the percent of CD4+ mesenteric lymphocytes and a decrease in the percent of CD8+ mesenteric lymphocytes when examined immediately after the cessation of IS. The stressor reduced antibody production to antigen processed at the altered mesenteric nodes, but did not alter antibody production to antigen processed at other sites. No measurable shifts were found in other compartments examined. The changes in CD4+ and CD8+ mesenteric lymphocytes resulted in an increased CD4+/CD8+ ratio that persisted for 1-24 h after stressor termination, becoming absent 48 h after IS termination. The stress-induced reduction in antibody production occurred only when antigen was given immediately prior to but not when antigen was given 48 h post stress. These findings suggest that the effects of a stressor could be specific to the manner in which the antigen enters the body, and that the stress-induced decrease in antibody production could be due to altered lymphocyte subpopulations as reflected by an increased CD4+/CD8+ ratio.