RESUMO
The ability of human lymphocytes and mouse splenocytes to secrete corticotropin-releasing factor (CRF) in response to hyperthermia, hyperosmolarity and hypoxia has been shown. Both human T- and B-lymphocytes appear to have this ability. E. coli lipopolysaccharide and concanavalin A can stimulate CRF secretion by B- and T-lymphocytes, respectively, whereas hydrocortisone inhibits the CRF secretion induced by any agent tested. Adrenocorticotropic hormone (ACTH) secretion in response to hyperthermia, hyperosmolarity and hypoxia was demonstrated also, and this secretion could be inhibited by anti-CRF antibodies and by hydrocortisone. We demonstrate that CRF could provide a necessary link between external stimuli such as cellular stress factors and ACTH secretion by immunocytes leading to corticosteroid production and, subsequently, to non-specific defence reaction of the organism. We also describe a model designed to explain the results obtained.