TH17 cell induction through IL-21-Ape1/Ref-1 pathway

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We found that IL-21 induced Ape1/Ref-1 protein and that the redox regulatory activity of Ape1/Ref-1 was essential for IL-21-induced ERK1/2 activation. To investigate the functional role of Ape1/Ref-1 in T cell differentiation and activation, we treated CD4^+ T cell with Ape1/Ref-1 redox inhibitor. The inhibitor upregulated IFN-. production from CD4^+ T cell, therefore Ape1/Ref-1 might control TH1/TH17 balance. We are now researching that the inhibitor can modulate DSS-induced colitis in IL-21isoform transgenic mice, which show more severe phenotype of colitis with TH17 cell accumulation than the wild type mice.