Abstract
Magnesium-dependent functions in the synthesis, release, and activity of cells of the immune system have been reported from in vivo and in vitro studies. Magnesium deficiency in animals is associated with impaired function of both humoral and cell-mediated immunity. Production and activity, including cell adhesion, of granulocytes and mononuclear phagocytes are affected by the availability of magnesium. Levels of immunoglobulin G (IgG) may be reduced, and IgE increased during magnesium deficiency. The latter observation suggests a role for magnesium in immediate hypersensitivity which is supported in some studies. Complement activation by the alternative pathway, but perhaps also by the classical pathway, is magnesium-dependent. Data indicate a role for magnesium in the proliferation and function of lymphocytes. For example, magnesium is required for the adhesion-recognition phase of the cytolytic T lymphocyte (CTL) reaction. Under some circumstances, magnesium may be anticarcinogenic, while under others, it may promote tumor growth. In spite of this exception, magnesium is a vital nutrient for optimal immune function.