Title |
Delphinidin Activates NFAT and Induces IL-2 Production Through SOCE in T Cells
|
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Published in |
Cell Biochemistry and Biophysics, August 2013
|
DOI | 10.1007/s12013-013-9728-z |
Pubmed ID | |
Authors |
Evelyn Jara, María A. Hidalgo, Juan L. Hancke, Alejandra I. Hidalgo, Sebastian Brauchi, Luisa Nuñez, Carlos Villalobos, Rafael A. Burgos |
Abstract |
Delphinidin is an anthocyanidin that possesses antioxidant and anti-inflammatory effects; however, some reports suggest that delphinidin has pro-inflammatory properties. For this reason, we assessed the effect of delphinidin on cytokine production in T cells. We demonstrated that delphinidin increased the cytosolic-free Ca(2+) concentration by releasing Ca(2+) from intracellular stores and increasing Ca(2+) entry. The putative Ca(2+) release activated Ca(2+) (CRAC) channel inhibitors BTP2 and gadolinium reduced the calcium entry stimulated by the anthocyanidin. Delphinidin induced nuclear factor of activated T cells (NFAT) translocation and NFAT-Luc activity in Jurkat cells and was dependent on the CRAC channel and calcineurin pathway. Delphinidin increased the mRNA expression and production of IL-2 in Jurkat cells and was inhibited by BTP2 and cyclosporine A. Using peripheral blood lymphocytes, we demonstrated that delphinidin increased the production of IL-2 and IFN-γ and was inhibited by BTP2. Taken together, our results suggest that delphinidin exerts immunostimulatory effects on T cells by increasing cytokine production through CRAC channel and NFAT activation. |
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