| Project/Area Number |
10470381
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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 | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
SAITO Ichiro The University of Tokushima, School of Dentistry, Associate Professor, 歯学部, 助教授 (60147634)
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| Co-Investigator(Kenkyū-buntansha) |
TSUBOTA Kazuo Tokyo Dental collage, Department of Ophthalmology, Professor, 眼科学, 教授 (40163878)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥9,300,000 (Direct Cost: ¥9,300,000)
Fiscal Year 1999: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1998: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | Sjogren's syndrome / Epstein-Barr virus / autoantigen / virus reactivation / apoptosis / シェ-グレン症候群 / エプスタイン・バ-ウイルス / EBウイルス |
|---|
| Research Abstract |
Sjogren's syndrome (SS) is an organ-specific autoimmune disease characterized by exocrine gland destruction, and Epstein-Barr virus (EBV) has been implicated in the pathogenesis of SS. The 120-kD a-fodrin may be a specific autoantigen in the pathogenesis of SS, but the mechanisms of a-fodrin cleavage leading to autoantigen formation remain unclear. A striking correlation between antibodies against 120-kD a-fodrin and a reactivated EBV antigen was found in sera from patients with SS, but not in those from normal individuals. To study whether EBV activation could induce the 120-kD a-fodrin, Akata cells were analyzed by immunoblot method. EBV-activated Akata cells had specific a-fodrin cleavage to the expected 120-kD fragments. Furthermore, caspase inhibitors inhibited the 120-kD a-fodrin cleavage. Thus, these results indicate that EBV reactivation may play an important role in the progression of a-fodrin cleavage by induction of apoptotic protease activities and the development of SS.
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