The present study investigated the question if a pharmacological blockade of cortisol release with stress affects lymphocyte redistribution in healthy volunteers. It was expected that the well known increases in the number of CD8+ (T-suppressor/cytotoxic cells) and CD56+ (natural killer cells) after stress would not be downregulated in the absence of an appropriate cortisol response, since redistribution is markedly influenced by glucocorticoids. In a double blind design, forty healthy male volunteers were exposed to a brief psychological stressor (public speaking) and received a single oral dose of dexamethasone [DEX] (N=20) or placebo (N=20) the evening before the main experiment. Ratings on emotional states and blood samples for determination of hormones, CD8+, and CD56+ cell counts were obtained at different time points during the experiment. Stress of public speaking led to highly significant increases in catecholamine and cortisol concentrations, to subjective discomfort and, most pronounced, to high increases in the number of CD8+ and CD56+ cells. DEX neither influenced baseline levels of mood, catecholamines and cell numbers nor stress induced responses of mood and catecholamines. However, during the whole experiment cortisol concentrations were suppressed in the DEX-condition and the number of CD8+, but not CD56+, cells remained elevated at the end of the session, while in the placebo condition the numbers of these cells were decreased to baseline levels. The data demonstrate that cortisol seems to play an important role in stress induced redistribution patterns of CD8+ but not CD56+ cells. This, however, can be explained by different migration processes between those cells (e.g. different targets of migration) and, therefore, different glucocorticoid influences on target tissues.