Grace A. Goldsmith Award lecture. Trace element regulation of immunity and infection

Abstract

Protein-calorie malnutrition is associated with impaired immunocompetence and increased susceptibility to infection. Clinically evident nutritional deficiency syndromes, however, are composite of deficits of many essential nutrients, each of which may exert an important regulating effect on immunity. Among other nutrients, several trace elements have been shown to regulate immune responses, particularly cell-mediated immunity. Zinc undernutrition results in lymphoid atrophy and reduced capacity to respond to many T-cell-dependent antigens. Plaque forming cell response to heterologous erythrocytes is decreased, as is the function of B cells. In zinc deficient rodents, the generation of cytotoxic lymphocytes in the spleen is reduced. Antibody-dependent cell-mediated cytotoxicity is largely unchanged. In acrodermatitis enteropathica, lymphocyte proliferation response to mitogens is decreased and there are significant changes in delayed hypersensitivity responses and in the proportion of various T cell subsets. Neutrophil function is not changed by zinc deficiency. Iron deficiency results in a slight decrease in the number of rosette-forming T cells and a significant impairment of lymphocyte response to mitogens and antigens. Polymorphonuclear leukocytes are unable to kill ingested bacteria and fungi in an efficient manner. Copper deficiency impairs cell-mediated immunity, as does selenium deficiency when it is associated with vitamin E lack. Several pathogenetic mechanisms may underlie such alterations in immunity. Many heavy metals impair immune responses. These effects of trace elements on immunity may have important fundamental and practical implications.