Lithium, known best for its efficacy in the treatment of neuropsychiatric disorders, also is capable of influencing the function of a variety of non-neural cells. Shenkman et al. (1978), for example, demonstrated that lithium was capable of enhancing several functions of human peripheral blood mononuclear cells. Lithium chloride, in vitro, augmented thymidine incorporation by phytohemagglutinin-stimulated human lymphocytes and increased the ability oi these cells to form rosettes with sheep erythro-cytes. Lithium also stimulated phagocytosis of polystyrene latex particles by cultured human macrophages. Finally, lithium was found capable of reversing the inhibitory effects of prostaglandin E1 and theophylline on the response of human lymphocytes to phytohemagglutinin. Since these inhibitory effects were very likely mediated by increased cellular levels of cyclic 3′,5′-adenosine monophosphate (cAMP), the authors concluded that lithium acted by interfering in some fashion with adenylate cyclase activity. A similar conclusion was reached more recently by Gelfand et al. (1979). These authors found that theophylline, salbutamol, isoproterenol, and dibutyryl cAMP inhibited sheep erythrocyte rosette formation by human T lymphocytes as well as secretion of immunoglobulin M from plaque-forming B cells. Consistent with an ability to inhibit adenylate cyclase, lithium prevented the effects of all the drugs except dibutyryl cAMP.