| Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2011: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2010: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2009: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Research Abstract |
In order to clarify the role of NF-kB in the pathogenesis of psoriasis, we examined whether pathological change of psoriasis was induced in IkBNS deficient mice. We also clarified the function of Bcl-3 in cultured epidermal keratinocytes. Although the IkBNS deficient mice did not spontaneously generate psoriatic skin phenotype, the psoriasis pathological change was induced by the wound stimulus and the TPA treatment. IL-22-induced psoriasis-related genes were suppressed by the pretreatment of Bcl-3 suppression. On the other hand, overexpression of Bcl-3 induced psoriasis-related gene expression. Furthermore, Bcl-3 was strongly detected psoriatic skin. In conclusion, NFkB and Bcl-3 play important roles in the pathogenesis of psoriasis.
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