Role of intracellular redox in crosstalk between TH1/TH2 balance and nature immunity

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We recently demonstrated that balance of reduced and oxidized glutathione level (GSH/GSSG) in macrophage (MΦ) play a central role in determining which of the TH1 and TH2 cytokine responses predominate during immune states through IL-12 production. In this study, we investigated whether changes in intra-cellular GSH/GSSG balance regulate LPS-induced IL-12 production and defined the molecular mechanism that underlies glutathione redox regulation.Glutathione redox regulates LPS-induced IL-12 production through p38 MAP kinase activation. (Ref 5) On the other hand, c-jun N-terminal kinase negatively regulates LPS-induced IL-12 production from MΦ, and glutathione redox regulates LPS-induced IL-12 production through the opposite control of JNK and p38 MAP kinase activation. (Ref 1)And, we revealed that TH1 and TH2 cytokines up and down-regulated the expression of Toll-like receptor 4 respectively, and that the crosstalk between TH1・TH2 balance and innate immunity. (Ref 3)Furthermore, TGF-β 1-induced CTGF mRNA expression in human lung fibroblasts is mediated through the JNK-dependent pathway. (Ref 2)