| Project/Area Number |
12670307
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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 |
Immunology
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| Research Institution | Juntendo University |
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Principal Investigator |
MATSUOKA Shuji Dept. Pathology, Juntendo University, Research Asistant, 医学部, 助手 (20286743)
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| Co-Investigator(Kenkyū-buntansha) |
TSURUI Hiromichi Dept. Pathology, Juntendo University, Research Asistant, 医学部, 助手 (40217386)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | RE2 / MHC class l / apoptosis / fulminant hepatitis / cell death / atopy |
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| Research Abstract |
We earlier found that a rat monoclonal antibody (mAb) RE2 can induce rapid death of murine activated, but not resting, lymphocytes in a complement independent manner, a cell death differing from typical apoptosis or necrosis. We here found that this cell death is independent of pathways involving Fas, caspase. We found that RE2 epitope resides on the murine class I a2 domain. However, the a3 domain plays a key role in transducing the death signal, which mediates extensive aggregation of the MHC class I- integrinactin filament system, giving rise to membrane pores. In mouse models with T cell activation- associated fulminant hepatitis, administration of mAb RE2 almost completely inhibited the development of liver cell injuries. Induction of this form of cell death using the mAbs may be potentially therapeutic for subjects with immunological diseases.
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