Cellular Immunotherapy for Pathological Retinal Neovascularization
| Project/Area Number |
17591851
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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 |
Ophthalmology
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| Research Institution | KEIO UNIVERSITY |
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Principal Investigator |
ISHIDA Susumu Keio University, School of Medicine, Assistant Professor, 医学部, 講師 (10245558)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAKAMI Yutaka Keio University, School of Medicine, Professor, 医学部, 教授 (50161287)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | angiogenesis / immunity / VEGF / retina / AMD / 加齢黄斑変性 |
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| Research Abstract |
Age-related macular degeneration (AMD) is the most common cause of blindness in the elderly people over the age of 50 in the developed countries. AMD is complicated by choroidal neovascularization (CNV), during which the choroidal new vessels invade the subretinal space through Bruch's membrane to form the fibrovascular proliferative tissue containing vascular endothelial cells, fibroblasts, retinal pigment epithelial (RPE) cells and various inflammatory cells. Our recent reports demonstrated CD8+ cytotoxic T cell (CTL)-mediated suppression of physiologic and pathologic retinal new vessels. In tumor models, specific immunization targeting VEGFR2, which are highly expressed in endothelial cells, was reported to inhibit tumor growth and angiogenesis. Accordingly, we hypothesized a possible immunological therapy for CNV by inducing CTL responses targeting VEGFR2, which is a specific molecule highly expressed in CNV-associated endothelial cells. Thus, we examined whether experimental CNV is suppressed by inducing specific cellular immunity against VEGFR2 via vaccination with dendritic cells (DCs), professional antigen-presenting cells.
In the paper already submitted, we showed, for the first time to our knowledge, that the induction of peptide-specific cellular immunity targeting endothelial cells inhibits CNV generation. Vaccination of DCs pulsed with the epitope peptide VEGFR2400-408 elicited the CTL responses specific for the peptide. Additionally, CD8 T cells were shown as the major effectors in the immunological treatment. These data indicate the new concept of CTL-mediated specific immunotherapy for CNV.
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Report
(3 results)
Research Products
(15 results)
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[Journal Article] Angiotensin II type 1 receptor-mediated inflammaton is required for choroidal neovascularization.2006
Author(s)
Nagai N, Oike Y, Izumi-Nagai K, Urano T, Kubota Y, Noda K, Ozawa Y, Inoue M, Tsubota K, Suda T, Ishida S.
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Journal Title
Arteriosclear Thromb Vasc Biol 26
Pages: 2252-2259
Related Report
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[Journal Article] Suppression of ocular inflammation in endotoxin-induced uveitis by inhibiting nonproteolytic activation of prorenin.2006
Author(s)
Satofuka S, Ichihara A, Nagai N, Yamashiro K, Koto T, Shinoda H, Noda K, Ozawa Y, Inoue M, Tsubota K, Suzuki F, Oike Y, Ishida S.
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Journal Title
Invest Ophthalmol Vis Sci 47
Pages: 2686-2892
Related Report
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