| Project/Area Number |
24790399
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Parasitology (including Sanitary zoology)
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| Research Institution | Gunma University |
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Principal Investigator |
IMAI Takashi 群馬大学, 医学(系)研究科(研究院), 助教 (10513434)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | マラリア / CD8 / マラリア原虫 / マクロファージ / 感染防御 / T細胞 / 赤芽球 / 赤内期 / 感染免疫 / CD8T細胞 / 貪食細胞 / 細胞傷害活性 / 防御免疫 |
|---|
| Research Abstract |
Mice depleted of CD8 T cells showed higher parasitemia and lower survival during infection with otherwise non-lethal blood-stage malaria parasites, indicating protective roles of CD8 T cells. However, how these cells mediate protection to blood-stage malaria parasites that infect red blood cells deficient in MHC class I expression is elusive. In this study, we found that erythroblasts, progenitor cells of red blood cells, are parasitized by malaria parasites, and parasitized erythroblasts were recognized by CD8 T cells in an antigen-specific manner, suggesting that parasitized erythroblasts are the target of CD8 T cell. We further explored protective mechanisms exerted by CD8 T cells. We revealed that phosphatidylserine was externalized on parasitized cells after a ligation of cytotoxic molecule FasL on CD8 T cells to Fas on the target cells, which leads to induce effective phagocytosis by macrophages.
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