ABSTRACT
This chapter explores the possible basis of the critical nature of the interaction of zinc with the immune system. Zinc is a ubiquitous trace metal essential to the development and maintenance of the immune system and influencing both lymphocyte and phagocyte cell functions. Various mechanisms can explain the early thymic atrophy observed in zinc-deprived mice. Rapidly replicating lymphocytes in the thymus could be particularly sensitive to the functional anomaly of zinc-rich metalloenzymes required for lymphocyte proliferation. The effects of zinc supplementation on thymic endocrine activity were particularly evident in aged patients with chronic renal failure, in whom the plasma thymulin levels during zinc treatment reached values usually found in normal young men. The antagonism between zinc and calcium would in fact be the result of the inhibitory effect of zinc on functions mediated by calmodulin. In addition, putative binding sites for zinc in the regulatory domain of protein kinase C have been proposed, suggesting an important role in cell activation.
