1998 Fiscal Year Final Research Report Summary
Analysis of signaling molecules for NK cell receptors
| Project/Area Number |
09670328
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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 |
Immunology
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| Research Institution | Chiba University Graduate School of Medicine |
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Principal Investigator |
ARASE Hisashi Chiba Univ., Grad.・Sch.of Med., Assistant, 医学部, 助手 (10261900)
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| Project Period (FY) |
1997 – 1998
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| Keywords | NKR-P1 / CD161 / CD16 / FcRgamma chain / ADCC / NK cell / IFN-gamma / CD3zetachain |
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| Research Abstract |
NKR-P1 molecule is thought to be one of activating receptor for NK cells and suggested to play an important role in cytotoxicity and IFN-gamma production by NK cells. Therefore, it is important to clarify the signaling mechanism of NKR-P1 molecule. In this study, in order to clarify the signaling pathway for NKR-P1 molecule, we analyzed association molecule for NKR-P1 and found that FcRgamma chain is associated with NKR-P1. Furthermore, analysis using FcRgamma-deficient mice revealed that FcRgamma is essential for signal transduction of NKR-P1.
On the other hand, NK cells are known to express CD3zetachain, a signal transducing molecule for TCR.However, the role of GD3zetaon NK cells has remained unclear, In order to analyze the function of CD3zeta expressed on NK cells, we purified NK cells from CD3zeta deficient mice and analyzed expression of various surface molecules. Then, we found that expression of FcgammaRIII is significantly high on NK cells from CD3zeta-deficient mice compared with that from normal mice. Furthermore, NK cells from CD3zeta-deficient mice produced a large amount of IFN-gammacompared with those from normal mice upon stimulation with FcgammaRIII crosslinking. These findings showed that CD3zetachain has an important role for the regulation of expression of FcgammaRIII on NK cells.
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