Effects of D2-dopamine and alpha-adrenoceptor antagonists in stress induced changes on immune responsiveness of mice.

The involvement of catecholamine receptors (alpha-adrenergic, D2-dopamine (DA)) was investigated in restraint stress influenced immune responses with concomitant changes of G-protein signal transduction. Impairment of the spleen morphology, TH1/TH2 cytokine network and natural killer (NK) cell function was observed. In vivo administration of specific antagonists prior to restraint stress reversed the immunosuppression. These findings demonstrate that D2-type dopaminergic mechanism represents the dominant component in regulation of Galphas/Galphai(1,2)/Galphaq/11-protein signal transduction and contribute to cell responses at postreceptor level of both, central nervous and immune systems. G-protein-coupled receptors (GPCRs) can modulate cytokine production and may play a regulatory role in immune effector mechanisms.