Experimental and clinical studies suggest that the central and peripheral benzodiazepine (BDZ) receptors together with their ligands form the molecular basis of a novel regulatory network that contributes to the effects of anxiety on immune status. The peripheral-type receptors located on phagocytes and glial cells appear to play a key role in mediating the effects of endogenous and exogenous BDZs both on the defence mechanisms that protect the host against pathogens and on inflammatory reactions that take place within the periphery and the brain in response to injury. In addition, the central-type receptor, which forms part of the gamma-aminobutyric acidA receptor complex, may contribute to the regulation of T-cell function by modulating the activity of the hypothalamo-pituitary-adrenocortical axis or the sympathoadrenal system or both, which, in turn, exert a significant effect on immune function. Thus, anxiogenic BDZs in general suppress the immune response, whereas anxiolytic BDZs may protect the individual from stress-induced immunosuppression.