Stress, cytokine patterns and susceptibility to disease

Recent evidence indicates that glucocorticoids and catecholamines, the end- products of the stress system, and histamine, a product of activated mast c ells, might selectively suppress cellular immunity, and favour humoral immu ne responses. This is mediated by a differential effect of stress hormones and histamine, on T helper I (Th1)/Th2 patterns and type I/type 2-cytokine production. Thus, systemically, stress might induce a Th2 shift, while, loc ally, under certain conditions, it might induce pro-inflammatory activities through neural activation of the peripheral corticotropin-releasing factor -mast cell-histamine axis. Through the above mechanisms, stress may influen ce the onset and/or course of infectious, autoimmune/ inflammatory, allergi c and neoplastic diseases.