An article published in the International Journal of Molecular Sciences stated that zinc homeostasis is crucial for adequate function of the immune system. Zinc deficiency and its excess lead to severe disturbances in immune cell numbers and activities, which can result in increased susceptibility to infections and development of especially inflammatory diseases.

This article was based on a review that focused on the role of zinc in regulating intracellular signaling pathways in innate, as well as adaptive immune cells. Zinc deficiency increases apoptosis within the B cell population and leads to cell depletion. Thus, there are fewer naïve B cells during zinc deficiency that can react to neoantigens. Zinc has a role in regulation of PTP and PT kinase (PTK) activity. Kinase and phosphatase activity are not only affected by intracellular zinc homeostasis, but both are involved in changing expression of genes relevant for regulation of zinc homeostasis. Long-term zinc deficiency increases the basal ROS levels and augments stimulation induced ROS synthesis in myeloid cells. A balanced zinc homeostasis is important to prevent unwanted signaling disturbances. Zinc deficiency increases interleukin (IL)-6-induced activation of JAK-STAT3 signaling pathways, while reconstitution with zinc normalizes the effect. Additionally, zinc supplementation has shown to inhibit STAT3 phosphorylation induced by IL-6 and IL-1. Zinc directly influences the biological activity of the thymic hormone thymulin by acting as an essential co-factor.

The authors summarized that all immune cells are directly affected by zinc signals. Most prominent pathologic changes are found during zinc deficiency indicating that zinc is a main regulator of cellular function and signal transduction.

Source: International Journal of Molecular Sciences. 2017 Oct 24;18(10):2222. doi: 10.3390/ijms18102222.