2004 Fiscal Year Final Research Report Summary
Basic Research for the Clinical Use of Nuclear Factor-binding DNA Decoy for Inflammatory Skin Diseases
| Project/Area Number |
14570800
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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 |
Dermatology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KOMINE Mayumi The University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (00282632)
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| Co-Investigator(Kenkyū-buntansha) |
KAKINUMA Takashi The University of Tokyo, Faculty of Medicine, Assistant, 医学部附属病院, 助手 (30332604)
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| Project Period (FY) |
2002 – 2004
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| Keywords | Keratinocytes / Chemokines / TARC / CCL17 / NF kappa B / STAT1 / Inflammatory skin diseases / Mechanical Stress / MAP kinases |
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| Research Abstract |
Thymus and activation-regulated chemokine (TARC/CCL17) is a potent chemokine, deeply associated with the pathogenesis of several inflammatory skin diseases, such as atopic dermatitis and bullous pemphigoid. Production of TARC from HaCaT keraitnocytes was synergistically induced by the stimulated with TNFα and IFNγ. NFkB and p38 are indispensable, EGF receptor was negatively involved, and STAT1 was not involved in this induction. PLA2 inhibitor, MAFP, and leukotrien B4 receptor inhibitor, LY, was also effective in suppressing TARC production. IMD, which was produced to suppress NFkB activation was effective in suppressing TARC production from HaCaT keratinocytes. Mechanical stress, are IL-15 are known to induce new lesions in psoriasis. They induced MAP kinase activation, proliferation, and attenuates apoptosis. Mechanical stress induced EGFR phosphorylation, ERK, and AP-1 activation. IL-15 induced ERK and PI3K activation. Suppression of these signaling molecules could be effective in treating inflammatory skin diseases such as psoriasis. We are planning to utilize these possibilities in vivo experiments.
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Research Products
(14 results)
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[Journal Article] Significant elevation of serum levels of eotaxin-3/CCL26, but not of eotaxin-2/CCL24, in patients with atopic dermatitis : serum eotaxin-3/CCL26 levels reflect the disease activity of atopic dermatitis.2003
Author(s)
Kagami S, Kakinuma T, Saeki H, Tsunemi Y, Fujita H, Nakamura K, Takekoshi T, Kishimoto M, Mitsui H, Torii H, Komine M, Asahina A, Tamaki K.
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Journal Title
Clin Exp Immunol. 134(2)
Pages: 309-313
Description
「研究成果報告書概要(欧文)」より
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[Journal Article] Increased serum cutaneous T cell-attracting chemokine (CCL27) levels in patients with atopic dermatitis and psoriasis vulgaris.2003
Author(s)
Kakinuma T, Saeki H, Tsunemi Y, Fujita H, Asano N, Mitsui H, Tada Y, Wakugawa M, Watanabe T, Torii H, Komine M, Asahina A, Nakamura K, Tamaki K.
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Journal Title
J Allergy Clin Immunol. 111(3)
Pages: 592-597
Description
「研究成果報告書概要(欧文)」より
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[Journal Article] IL-4, but not IL-13, modulates TARC (thymus and activation-regulated chemokine)/CCL17 and IP-10 (interferon-induced protein of 10kDA)/CXCL10 release by TNF-alpha and IFN-gamma in HaCaT cell line.2002
Author(s)
Kakinuma T, Nakamura K, Wakugawa M, Yano S, Saeki H, Torii H, Komine M, Asahina A, Tamaki K.
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Journal Title
Cytokine. 20(1)
Pages: 1-6
Description
「研究成果報告書概要(欧文)」より
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