Zinc up-regulates NF-κB activation via phosphorylation of IκB in HUT-78 (Th 0) cells

Abstract

Nuclear factor of κB (NF-κB) is a major transcription factor regulating the expression of interleukin-2 (IL-2) and interleukin-2 receptor-α (IL-2Rα) in Th 1 cells. We previously demonstrated that zinc increased IL-2 and IL-2Rα production via NF-κB activation in HUT-78 (Th 0) cells. However, the molecular mechanism is not well understood. In this study, we found that zinc increased phosphorylated IκB-α, NF-κB translocation and activation, as well as the production of IL-2 and IL-2Rα in wild type IκB gene transfected zinc-sufficient HUT-78 cells, compared to zinc-deficient HUT-78 cells. However, dominant negative IκB gene expression decreased these parameters in zinc-sufficient cells, suggesting that zinc increased NF-κB activation via IκB pathway.