Selenium and immune responses.
Selenium (Se) affects all components of the immune system, i.e., the development and expression of nonspecific, humoral, and cell-mediated responses. In general, a deficiency in Se appears to result in immunosuppression, whereas supplementation with low doses of Se appears to result in augmentation and/or restoration of immunologic functions. A deficiency of Se has been shown to inhibit resistance to microbial and viral infections, neutrophil function, antibody production, proliferation of T and B lymphocytes in response to mitogens, and cytodestruction by T lymphocytes and NK cells. Supplementation with Se has been shown to stimulate the function of neutrophils, production of antibodies, proliferation of T and B lymphocytes in response to mitogens, production of lymphokines, NK cell-mediated cytodestruction, delayed-type hypersensitivity reactions and allograft rejection, and the ability of a host to reject transplanted malignant tumors. The mechanism(s) whereby Se affects the immune system is speculative. The effects of Se on the function of glutathione peroxidase and on the cellular levels of reduced glutathione and H2Se, as well as the ability of Se to interact with cell membranes, probably represent only a few of many regulatory mechanisms. The manipulation of cellular levels of Se may be significant for the maintenance of general health and for the control of immunodeficiency disorders and the chemoprevention of cancer.
D000818:Animals; D002462:Cell Membrane / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000032:analysis; D006801:Humans; D007109:Immunity / Q000187:drug effects*; D012643:Selenium / Q000172:deficiency / Q000378:metabolism / Q000494:pharmacology*
D005979:Glutathione Peroxidase; D005978:Glutathione; D012643:Selenium