| Project/Area Number |
08672039
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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 | NIPPON MEDICAL SCHOOL |
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Principal Investigator |
OHARA Kunitoshi SCHOOL OF MEDICINE,NIPPON MEDICAL SCHOOL PROFESSOR, 医学部, 教授 (00137704)
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| Co-Investigator(Kenkyū-buntansha) |
IBARAKI Nobuhiro SCHOOL OF MEDICINE,NIPPON MEDICAL SCHOOL ASSOCIATE PROFESSOR, 医学部, 助教授 (90240986)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | AGE-RELATED CATARACT / AUTOIMMUNE / HUMAN LENS EPITHELIAL CELL CULTURE / BETA-CRYSTALLIN / COMPLEMENT / CELL DEATH / DIFFERENTIATION / HUMAN SERA / ベータ-・クリスタリン / 細胞障害 |
|---|
| Research Abstract |
Circulating autoantibodies against lens antigens are prevalent in patients with age-related cataract (ARC), but their pathogenic significance is unknown. We hypothesized that these autoantibodies are cytotoxic for lens epithelial cells (LECs). To test this hypothesis, we incubated LECs with mouse polyclonal antibodies against beta-crystallin (anti-beta) in the presence or absence of guinea pig complement. We found that anti-beta in the presence of the complement bound to and killed human LECs (HLECs). Sera obtained from patients with ARC also were cytotoxic to HLECs. These results support the hypothesis that autoantibodies against lens antigens are cytotoxic to LECs, and that cell death may involve complement-mediated pathways.
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