RESUMO
The purpose of this study was to analyze the effect of fluoxetine upon human T lymphocyte proliferation, and to assess the early signals elicited after T cell triggering and cAMP formation. Blood samples from normal human volunteers were drawn from venipuncture and T cells were cultured in the presence or absence of Concanavalin A (Con A) and fluoxetine. Protein Kinase C (PKC) levels and cyclic adenosine monophosphate (cAMP) formation were also measured. Fluoxetine exerted dual effect, depending on the degree of lymphocyte activation: at mitogenic concentrations of Con A (2 mug/ml), we observed na inhibitory effect on cellular proliferation. This inhibitory effect involves PKC degradation and cAMP formation. On the other hand, when submitogenic Con A concentrations (1mug/ml) were used, fluoxetine stimulated the cellular response and increased PKC traslocation. The participation of extracellular calcium mobilization could be involved in these mechanisms. According to our results, fluoxetine seems to modulate calcium influx which, in turn, would influence PKC traslocation, thus modulating the immune response through a mechanism that could be involving cAMP participation.