| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Psoriasis is a common chronic inflammatory skin disease. Recently, the IL-1 family members Interleukin-36, IL-36alpha, IL-36beta, IL-36gamma and the receptor antagonist IL-36Ra, constitute a novel signaling system that is poorly understood. First, we verified that psoriatic lesions showed increased levels of IL-36 ligands. Next, psoriasis like lesions in this K5.Stat3C mice showed increased transcriptional levels of the IL36A, IL36B, IL36G and IL36RN. To verify whether IL-36R deficiency attenuated psoriasis-like lesion of mice model, we generated IL-36R(-/-):K5.Stat3C mice. Strikingly, IL-36R deficiency markedly attenuated TPA-induced skin lesion, regarding ear thickness and histology. In addition, IL-23p19, and other signature molecules related with psoriasis were down-regulated. Finally, experiments using primary kerarinocytes(KC), dendric cells(DC) and bone marrow chimera mice, revealed that the IL-36 signalings of both KCs and DCs contributed to development of psoriatic lesion.
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