Abstract
The immune and neuroendocrine systems are clearly interrelated via a bidirectional network through which hormones and neuropeptides affect immune function and, in turn, immune responses are reflected in neuroendocrine changes (1-5). This tight communication between the two systems is made possible because both systems speak a common “ chemical language ” by sharing a common set of ligands and receptors of classical hormones, neuropeptides and immunoregulatory mediators. Indeed, in addition to possessing more than 30 different types of hormonal receptors classically associated with endocrine tissues, the cells of the immune system do synthesize and secrete numerous hormones and neuropeptides (6-11). Over the last years, it has been suggested that in addition to the well known immunosuppressive effects of adrenal glucocorticoids, many hormones are able to modulate immune processes. For example, hypothalamic factors such as the corticotropin-releasing-hormone (CRH) and somatostatin as well as pituitary hormones such as growth hormone (GH) and prolactin (PRL) can modulate the immune function. Indeed, CRH, the major stress-integrating peptide, which primarily stimulates ACTH secretion, does also act centrally as an immunosuppressant agent, independent of circulating glucocorticoids (12–14). Among other effects, it reduces natural killer cells activity as well as T-lymphocyte proliferation. This central immunosuppressive effect of CRH seems to be mediated via the central sympathetic nervous system. Keywords Migration Inhibitory Factor Leukemia Inhibitory Factor ACTH Release Splenocyte Culture Leukemia Inhibitory Factor Gene These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.