Investigation of pathological mechanism of bullous pemphigoid and development of new treatment
| Project/Area Number |
20591337
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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 | University of Toyama |
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Principal Investigator |
SHIMIZU Tadamichi University of Toyama, 大学院・医学薬学研究部(医学), 教授 (70260396)
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| Co-Investigator(Kenkyū-buntansha) |
MAKINO Teruhiko 富山大学, 大学病院, 講師 (90359711)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 水疱性類天疱瘡 / サイトカイン / ケモカイン / 自己抗体 / MIF / 炎症 / 水疱 / エラスターゼ / 水疱性類疱瘡 / 水庖性類天庖瘡 / 水庖 |
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| Research Abstract |
Bullous pemphigoid (BP) is an inflammatory subepidermal blistering disease associated with an autoimmune response to two hemidesmosomal antigens, BP230 and BP180. We analyzed the role of cytokines in the pathogenesis of BP.
We first found that the Macrophage migration inhibitory factor (MIF) levels in the serum and blister fluid were significantly elevated in BP patients and the serum MIF levels decreased in accordance with the improvement of BP. Liu et al have previously reported a murine model of BP, induced by a passive transfer of anti-mice BP180 NC16a antibodies. MIF transgenic (Tg) mice and MIF knockout (KO) mice were used to assess the potential role of MIF in the pathogenesis of BP in this murine model of BP. The blister formation in MIF TG mice showed no difference from that of WT mice after an injection of anti-mice BP180 NC16a antibodies. On the other hand, the blister formation in MIF KO mice markedly decreased in comparison with that of wild type mice after an injection of anti-mice BP180 NC16a antibodies. These results suggest that MIF might be involved in the pathogenesis of BP via both the inflammation of the epidermis and the infiltration of various cells, such as eosinophils
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Report
(4 results)
Research Products
(83 results)
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[Journal Article] Bone marrow transplantation restores epidermal basement membrane protein expression andrescues epidermolysis bullosa model mice.2011
Author(s)
Fujita Y, Abe R, Inokuma D, Sasaki M, Hoshina D, Natsuga K, Nishie W, McMillan JR, Nakamura H, Shimizu T, Akiyama M, Sawamura D, Shimizu H.
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Journal Title
Proc Natl Acad Sci USA. 107
Pages: 14345-14350
Related Report
Peer Reviewed
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[Journal Article] DNA-vaccination against macrophage migration inhibitory factor improves atopic dermatitis in murine models.2009
Author(s)
Hamasaka A, Abe R, Koyama Y, Yoshioka N, Fujita Y, Hoshina D, Sasaki M, Hirasawa T, Onodera S, Ohshima S, Leng L, Bucala R, Nishihira J, Shimizu T, Shimizu H.
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Journal Title
J Allergy Clin Immunol 124
Pages: 90-99
Related Report
Peer Reviewed
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[Journal Article] Interleukin-1βand macrophage migration inhibitory factor (MIF) in dermal fibroblasts mediate UVA induced matrix metalloproteinase-1 expression.2008
Author(s)
Honda A, Abe R, Makino T, Norisugi O, Fujita Y, Watanabe H, Nishihira J, Yamagishi S, Iwakura Y, Shimizu H, Shimizu T.
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Journal Title
J Dermatol Sci. 49
Pages: 63-72
Related Report
Peer Reviewed
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