Zinc plays a pivotal role in the immune system. Zinc-deficient individuals might experience increased susceptibility to a diversity of pathogens. The immunological mechanisms by which zinc regulates increased susceptibility to infection have long been studied. It is very clear that zinc affects several aspects of the immune system, starting from the barrier of the skin to gene regulation within lymphocytes.

Zinc is very important for normal development and function of cells that mediate nonspecific immunity, for example neutrophils and natural killer cells. Deficiency of zinc affects development of acquired immunity by inhibiting both the outgrowth and certain functions of T lymphocytes, for instance, activation, Th1 cytokine production, and B lymphocyte support. Also, B lymphocyte development and the antibody production, mostly the immunoglobulin G, is compromised.

The macrophage, which is a pivotal cell in several immunologic functions, is also adversely affected by zinc deficiency. It can dysregulate intracellular killing, phagocytosis and cytokine production. The effects of zinc supplementation on these immunologic mediators is deep-rooted in the countless roles for zinc in basic cellular functions as DNA replication, RNA transcription, cell activation and cell division. Apoptosis is also potentiated by zinc deficiency. Zinc functions as an antioxidant and can also stabilize membranes. Thus, in this review various aspects of zinc biology in the immune system and its attempts to offer a biological basis for the altered host resistance to infections during zinc deficiency and supplementation are explained.

Source: Shankar AH, Prasad AS. Zinc and immune function: the biological basis of altered resistance to infection. Am J Clin Nutr. 1998;68(2 Suppl):447S-463S. doi:10.1093/ajcn/68.2.447S

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