By virtue of their functional antagonism, Thl cells or cells producing the same cytokines as Thl cells may behave as 'suppressor cells' with respect to Th2 cells and vice versa. An excessive Th1- or Th2-like response may favor the development of different autoimmune diseases. As can be expected from their physiological role, Th-1 cytokines participate in autoimmune diseases with a preferential delayed type hyper-sensitivity component, i.e. in those diseases in which cytotoxic T cells attack organ-specific target cells. Autoimmune diseases with a predominant Thl component include experimental autoimmune encephalitis and insulin-dependent diabetes mellitus. In contrast, Th2-type responses participate in systemic autoimmune diseases with a strong humoral component. Such diseases probably include certain drug-induced states of autoaggression, namely mercury-induced autoimmune disease and chlorpromazine-induced autoimmunity. It is tempting to speculate that therapeutic interventions designed to recover a normal Thl/Th2 balance will provide a useful etiological strategy for the re-establishment of self-tolerance.