Animal studies in the 1930s first documented the essential requirement of zinc (Zn) for the growth and survival of animals (Todd et al., 1934). It was not until the 1960s that the importance of Zn deficiency for human populations was appreciated (see Prasad, 1991). Later, it became clear that Zn was also crucial for patients maintained on parenteral nutrition (Kay and Tasman-Jones, 1975). A central clinical feature of Zn deficiency in humans was the increased susceptibility to infectious diseases. Studies in the Middle East revealed that most Zn-deficient dwarfs succumbed to infections before they reached 25 years of age, leading researchers to speculate that Zn must be important for host immunity. The last two decades have witnessed a rapid growth in knowledge of the underlying mechanisms whereby Zn exerts its ubiquitous effects on immune function and disease resistance. The effects of Zn deficiency and of Zn supplementation on immune cells underscore the essential role of Zn in the normal development and function of many key tissues, cells and effectors of immunity. In vitro studies have elucidated the role of Zn at the cellular level and recent advances in molecular and cell biology have begun to clarify the role of Zn in gene expression, mitosis and apoptosis of lymphoid cells. It is clear that even mild Zn deficiency can impair multiple mediators of host immunity, ranging from the physical barrier of the skin to acquired cellular and humoral immunity (see Frost et al., 1977; Oleske et al., 1979; Good, 1981; Walsh et al., 1994).

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