The analysis of pathophysiology of autoimmune bullous diseases by using retrovirus vector
| Project/Area Number |
21791097
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Keio University |
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Principal Investigator |
KOHNO Michiyoshi Keio University, 医学部, 助教 (30403182)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 自己免疫 / T細胞受容体 / 皮膚炎 / サイトカイン / 免疫学 / シグナル伝達 |
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| Research Abstract |
Pemphigus vulgaris (PV) is an autoimmune bullous disease with circulating IgG autoantibodies against desmogleins (Dsg). We recently established Dsg3-specific T cell clones that induced PV phenotype and isolated cDNA clones of their T cell receptors (TCR). Herein, we retrovirally transduced wild type CD4^+ T cells with these TCR cDNAs (rvDsg3 T cells) to clarify their pathogenic roles for antigen-specific autoimmune processes in skin. When rvDsg3 T cells were transferred with Dsg3^<-/-> B cells into Rag2^<-/-> mice, the recipient mice neither showed clinical PV phenotype, anti-Dsg3 IgG production, nor histological evidence for acantholysis, but instead developed scaly and erythematous skin lesions. Histology revealed interface dermatitis only in skin, mucous membranes and esophagus, where Dsg3 was expressed.
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Report
(3 results)
Research Products
(5 results)
