| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Research Abstract |
To make clear the role of NKT2 cell and insulin resistance in the pathogenesis of autoimmune hepatitis, we performed our study and revealed following newly identified points.
1. NKT1 cell participated in active phase of AIH, on the contrary NKT2 cell participate in recovery phase of AIH.
2. The balance of NKT1 and NKT2 did not influence on the profile of intrahepatic CD8 nor regulatory T cells (Treg).
3. In active phase of AIH, the expression of DAMP receptor RAGE、TLR4、TLR9 were increased on CD4, CD8 cell, RAGE、TLR9 were increased on NKT1, NKT2 cell and Treg cells. This increase was mediated by inflammatory cytokines.
4. Insulin resistance participated in the chronic inflammation of AIH by enhancing Th1 cytokine production by CD4 cell and increasing number of NKT cell and enhancing Th1 cytokine production by NKT cell.
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