Premium
Zinc supplementation augments TGF‐β1‐dependent regulatory T cell induction
Author(s) -
Maywald Martina,
Meurer Steffen K.,
Weiskirchen Ralf,
Rink Lothar
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600493
Subject(s) - foxp3 , regulatory t cell , smad , immune system , transforming growth factor , intracellular , zinc , peripheral blood mononuclear cell , transforming growth factor beta , secretion , immunology , interleukin 10 , chemistry , biology , microbiology and biotechnology , t cell , endocrinology , il 2 receptor , biochemistry , in vitro , organic chemistry
Scope Regulatory T cells (Treg) play a pivotal role in immune regulation. For proper immune function, also trace elements such as zinc, and anti‐inflammatory cytokines, including transforming growth factor beta 1 (TGF‐β1) and interleukin (IL)‐10 are indispensable. Hence, in this study the influence of TGF‐β1, IL‐10, and zinc supplementation on Treg cells differentiation was investigated. Methods and results A synergistic effect of a combined zinc and TGF‐β1 treatment on Foxp3 expression in peripheral blood mononuclear cells and mixed lymphocyte cultures (MLC) was found by performing Western blot analysis. Additionally, combined treatment causes elevated Smad 2/3 phosphorylation, which plays an important role in Foxp3 expression. This is due to a TGF‐β1‐mediated increase of intracellular‐free zinc measured by zinc probes Fluozin3‐AM and ZinPyr‐1. Moreover, zinc as well as TGF‐β1 treatment caused significantly reduced interferon (IFN)‐γ secretion in MLC. Conclusion Combined zinc and TGF‐β1 treatment provoked an increased Treg cell induction due to a triggered intracellular zinc signal, which in association with an increased Smad 2/3 activation leads to a boosted Foxp3 expression and resulting in an ameliorated allogeneic reaction in MLC. Thus, zinc can be used as a favorable additive to elevate the induction of Treg cells in adverse immune reactions.