| Project/Area Number |
12672107
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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 |
Biological pharmacy
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MASTSUMOTO Naoki The University of Tokyo, Graduate school of Frontier sciences, Associate Professor, 大学院・新領域創成科学研究科, 助教授 (40239108)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Kazuo The University of Tokyo, Graduate school of Frontier sciences, Professor, 大学院・新領域創成科学研究科, 教授 (20174782)
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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 |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Keywords | NK cells / activating receptors / NKR-P1 / NKp46 / B cells / innate immunity / surface IgM / オーファンレセプター / Ly49 / ナチュラルキラー細胞 / リガンド / MHCクラスI |
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| Research Abstract |
Natural killer (NK) cells recognize target cells by activating as well as inhibitory receptors. However, our understanding of activating receptors is limited. In the current study we attempted to identify the ligands for the "orphan NK cell activation receptors", NKR-P1 and NKp46, of which ligands are unknown. By in vitro refolding of extracellular regions of the receptors expressed in E. coli, we succeeded in preparing soluble version of mouse NKR-P1 and mouse NKp46. To identify the NKR-P1 ligand we tested more than 50 cell lines for binding of soluble NKR-P1 to find out a B lymphoma line to bind soluble NKR-P1. We further produced a monoclonal antibody that inhibits NKR-P1 binding to the B lymphoma. Immunoprecipitation analysis of the putative NKR-P1 ligand recognized by the antibody suggests that the putative ligand is surface IgM. Indeed, polyclonal anti-IgM antibody inhibited NKR-P1 binding to the B lymphoma. These results clearly indicate that the NKR-P1 ligand on the B lymphoma cells is surface IgM. Exploration for normal B cell counterpart for the B lymphoma that binds soluble NKR-P1 revealed that a subset of B1 B cells also express NKR-P1 ligand. These data raise a novel possibility that NK cells and B1 B cells, both of which are player in innate immunity, may have unknown communication network.
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