| Project/Area Number |
08044284
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Field |
寄生虫学(含医用動物学)
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| Research Institution | Osaka University |
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Principal Investigator |
HORII Toshihiro Osaka University Res.Inst.Microbial Dis., Assoc.Professor, 微生物病研究所, 助教授 (80142305)
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| Co-Investigator(Kenkyū-buntansha) |
FOX Barbara A. Dartmouth Med.School, Senior Assoc.Researcher, 医学部, 上級研究助手
ARMAH GeorgeE. Noguchi Memo.Inst.Med.Res., GhanaUniv., Prof., 野口記念医学研究所, 主任研究員
HYDE John E. Univ.Manchester Inst.Sci.Tech., Senior lecturer, 上級講師
KRUNGKRAI Jerapan Churalongkon Univ., Faculty of Med., Assoc.Prof., 医学部, 助教授
BZIK David J. Dartmouth Med.School, Assoc.Professor, 医学部, 助教授
高橋 正行 キュリー研究所, 研究部長
森松 克実 大阪大学, 微生物病研究所, 助手 (70263308)
三田村 俊秀 大阪大学, 微生物病研究所, 助手 (80268846)
李 接 広東省衛生防疫站, 寄生虫病防治研究所, 研究員
BZIK David ダートマス大学, 医学部, 助教授
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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 |
¥12,000,000 (Direct Cost: ¥12,000,000)
Fiscal Year 1997: ¥5,700,000 (Direct Cost: ¥5,700,000)
Fiscal Year 1996: ¥6,300,000 (Direct Cost: ¥6,300,000)
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| Keywords | SERA / Malaria / P.falciparum / Vaccine / Complement / IgG / lgG / 熱帯熱マラリア / Plasmodium falciparum / マラリアワクチン / SERA抗原 / リスザル / 遺伝子多型 / マウスmAb / エピトープ解析 |
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| Research Abstract |
The Plasmodium falciparum SERA (113 kDa), one of the vaccine candidate antigens, is an asexual blood stage antigen produced in large amounts specifically during late trophozoite and schizonts stages. SERA is processed into 47 kDa, 50 kDa and 18 kDa fragments at the schizont rupture. We expressed N-terminal domain (SE47' ) of SERA protein in E.coli and showed that the recombinant protein induces parasite inhibitory antiserum. We purified SE47'-specific lgG by affinity chromatography to study molecular mechanisms of anti SERA anatibody to inhibit the parasite growth. The results were as follows ; 1) Affinity purified anti-SE47' IgG molecules efficiently inhibit the parasite growth. 2) Anti-SE47' IgG molecules agglutinate schizonts and merozoites, resulting in the growth inhibition of the parasite. 3) Complement-fixing subclasses lgGs are more potent in the inhibition than other subclass. 4) Active complement enhanced the parasite growth inhibition by anti SERA IgG and the resulted schizont contained degenerated nuclei, suggesting that the parasites were killed by the classical pathway of complement. These findings strongly support a feasibility of the recombinant SERA as a malaria vaccine.
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