| Project/Area Number |
14570403
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内科学一般
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| Research Institution | Gunma University |
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Principal Investigator |
DOBASHI Kunio Gunma University, School of Medicine, Assistant Professor, 医学部, 講師 (00241894)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | TH1 / TH2 balance / glutathione / IL-12 / oxidative stress / Toll-like receptor / GSH / GSSG / MAP kinase / レドックス / Th1・Th2バランス / MAPキナーゼ |
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| Research Abstract |
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)
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