Neuroimmunomodulation by Gonadotropin Releasing Hormone

Abstract

Gonadotropin-releasing hormone (GnRH) and GnRH receptor are produced locally by immune cells, suggesting an autocrine or paracrine role for GnRH within the immune system. The lymphocytes (T, B and NK cells), monocytes, macrophages, neutrophils, eosinophils and mast cells are affected directly or indirectly by GnRH. GnRH or GnRH agonists regulate immune cells, the expression of various receptors, cell proliferation, IFN␥ secretion, the adhesion proteins of extracellular matrix, chemotactic migration, the cell cytotoxicity, and angiogenic chemokines. IL-4 production is suppressed and both nitric oxide and nuclear factor-kappa B are inhibited. Furthermore, GnRH has been reported to exacerbate the responses in autoimmune diseases such as systemic lupus erythematosus, autoimmune thyroiditis and autoimmune diabetes. However, GnRH administration reduces the severity of experimental autoimmune encephalomyelitis. Thus, GnRH may modulate multiple functions involved in the immune system through the integration of a set of homeostatic mechanisms.