2001 Fiscal Year Final Research Report Summary
Evaluation of immune suppressive therapy using autoimmune model mouse
| Project/Area Number |
12557072
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Dermatology
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| Research Institution | Keio University |
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Principal Investigator |
NISHIKAWA Takeji Keio University School of Medicine, Professor, 医学部, 教授 (50051579)
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| Co-Investigator(Kenkyū-buntansha) |
KOYASU Shigeo Keio University School of Medicine, Professor, 医学部, 教授 (90153684)
ISHIKO Akira Keio University School of Medicine, Assistant Professor, 医学部, 専任講師 (10202988)
AMAGAI Masayuki Keio University School of Medicine, Assistant Professor, 医学部, 専任講師 (90212563)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Autoimmune / Autoantibody / Model mouse / Pemphigus / desmoglein / Immune suppression / Therapy / cadherin |
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| Research Abstract |
Treatment regime for rare diseases, such as autoimmune diseases, are mostly based on personal experiences and each treatment lacks objective evaluation. This is largely due to the lack of animal models which well mimic the corresponding human diseases. We have recently developed a novel active disease mouse model using autoantigen knockout mouse, which does not require immune tolerance against the defective autoantigen. The purpose of this study is to develop an evaluation system of various immune suppressive therapeutic strategies using the autoimmune disease mouse model. Dsg3 -/- mice, which originally had a mixed genetic background of 129 and C57BL/6 mouse, were backcrossed to C57BL/6 and Balb/C mouse by 10 generation to reduce the difference of immune response of each individual mouse. A large mouse colony was established to supply a sufficient number of model mice for this assay. An objective score to evaluate the disease activity of the model mouse considering number of skin lesions, weight loss and patchy hair loss. The usefulness of our system was confirmed by evaluating a novel therapeutic strategy using anti-CD40L monoclonal antibody. In the future various therapeutic strategies will be evaluated with our system using the model mouse
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