Figure 2.

Zinc is an integral part of a thymic hormone molecule, thymulin. Thymulin is required for maturation of T cells. Zinc deficiency-induced decrease in thymulin activity is associated with decreased maturation of T cells and Th1 production of IL-2 and INF-γ. Decreased IL-2 leads to decreased NK and T cytolytic cell activities. Macrophages–monocytes produce IL-12 (a zinc-dependent cytokine), which along with INF-γ kills parasites, viruses, and bacteria. Th2 cytokines, in general are not affected by zinc deficiency except IL-10, which may be increased in zinc-deficient elderly individuals. Increased IL-10 from Th2 cells further affects Th1 functions adversely. Thus, in zinc deficiency there is a shift from Th1 to Th2 functions and cell-mediated immune functions are impaired. Zinc deficiency also leads to stress and activation of macrophages–monocytes, resulting in increased generation of inflammatory cytokines, IL-1β, IL-6, IL-8, and TNF-α. Solid lines indicate pathways leading to generation of selected cytokines and dotted lines represent pathways, which lead to inhibition of cytokine generation. NK represent natural-killer cells; Th1 represent activated Th1 type T cells and secreted cytokines (small triangles); Th2 represents activated Th2 type T cells and secreted cytokines (small rounds); B-cell represents B-cell lineages and associated immunoglobulins (triangles). (Prasad, AS. Zinc: role in immunity, oxidative stress and chronic inflammation. Current Opinion in Clin Nutr and Metab Care, 12:646–652, 2009)