Zinc aspartate suppresses proliferation and Th1/Th2/Th17 cytokine production of pre-activated human T cells in vitro.

The essential trace element zinc, necessary for many biological processes of living organisms, plays a regulatory role in the maintenance of immune functions. Zinc deficiency affects components of both the innate and the adaptive immune system. On the other side, zinc is capable of suppressing activation and proliferation of human T cells. In the present study, we investigated the effect of zinc aspartate (Unizink®), an approved drug to treat zinc deficiency, on pre-activated human T cells (T cell blasts) in vitro. T cells of healthy donors were stimulated for 48 h with anti-CD3/CD28 antibodies. After this time period, zinc aspartate or the immunosuppressive drugs cyclosporin A, dexamethasone, and rapamycin were added for additional 24 h to these cell cultures. Subsequently, T cell proliferation and cytokine production was measured. In contrast to cyclosporine A and dexamethasone, only zinc aspartate and rapamycin were capable of suppressing the proliferation and Th1 (IFN-γ), Th2 (IL-5), and Th17 (IL-17) cytokine production of pre-activated T cells. This data suggest that zinc aspartate has the capacity to suppress proliferation and cytokine production of pre-activated human T cells in vitro. Thus, administration of zinc aspartate may have beneficial effects on T cell-mediated autoimmune diseases.