The present invention relates to the discovery that signaling via a serotonin type 1B, 2, 4 and 6 receptor is important in T cell activation such that inhibiting such signaling, such as by using fluphenazine, can be used to modulate the immune response, cell proliferation, and apoptosis, among other cell processes. This immunomodulation is useful for the treatment of immune diseases or conditions, and for the development of potential therapeutics for such diseases or conditions. It has been further discovered that, in cells proceeding through the cell cycle process, inhibition of serotonin signaling inhibits the process and induces apoptosis and morphological changes to a cell. These effects of inhibiting serotonergic signaling can be useful for effecting selective cell killing and for identifying compounds that inhibit the signaling. Additionally, methods for the use, identification and production of an inhibitor that does not substantially cross the blood-brain barrier are also provided.