Biomedical subjects
Publications and source records attributed to GP Chrousos.
Since the human glucocorticoid receptor (GR) cDNA and gene sequences were reported, the existence of two highly homologous GR isoforms was predicted. These were the classic human ligand-binding GRalpha, and a slightly smaller protein, termed GRbeta. Although the mechanism of action of GRbeta has been studied extensively, the role of GRbeta in the modulation of glucocorticoid actions remains uncertain.
In general, stress has been regarded as immunosuppressive. Recent evidence, however, indicates that acute, subacute or chronic stress might suppress cellular immunity but boost humoral immunity. This is mediated by a differential effect of stress hormones, the glucocorticoids and catecholamines, on T helper 1 (Th1)/Th2 cells and type 1/type 2 cytokine production. Furthermore, acute stress might induce pro-inflammatory activities in certain tissues through neural activation of the peripheral corticotropin-releasing hormone-mast cell-histamine axis. Through the above mechanisms, stress might influence the onset and/or course of infectious, autoimmune/inflammatory, allergic and neoplastic diseases.