| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Psoriasis is a helper T 17 cell-dependent chronic inflammatory skin disease characterized by thickening and redness of the skin with keratinocytes hyperproliferation, skin inflammation associated with inflammatory cell infiltration in the epidermis and dermis. Apoptosis signal-regulating kinase 1(ASK1) is a ubiquitously expressed serine/threonine mitogen-associated protein kinase kinase kinase (MAP3K) that activates p38 and JNK signaling pathways. In the present study, we investigated the role of ASK1 in the development of imiquimod-induced psoriasiform dermatitis by using ASK1 deficient mice. ASK1 deficient mice showed exacerbated psorisaiform dermatitis with increased expression of inflammatory cytokines such as TNF-α and IL-17 and proliferation of keratinocytes but decreased apoptosis of them. The present results suggest that ASK1 may play a role for supporting the normal differentiation of keratinocytes, which is presumed to be inhibitory against the development of psoriasis.
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