| Project/Area Number |
17590342
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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 |
Experimental pathology
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| Research Institution | Kyoto University |
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Principal Investigator |
TAKAHARA Kazuhiko Div. of Systemic Life Science, Grad. School of Biostudies., Lecturer, 生命科学研究科, 講師 (90301233)
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| Co-Investigator(Kenkyū-buntansha) |
INABA Kayo Div. of Systemic Life Science, Grad. School of Biostudies., Pfofessor, 生命科学研究科, 教授 (00115792)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | lectin / TLR4 / TLR2 / macrophage / Gram-negative bacteria / cytokine / Candida albicans / lipopolysaccharide / RAW264.7 / Zymosan / 樹状細胞 / TLR / 酵母 / DC-SIGN |
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| Research Abstract |
C-type lectins in immune system play a roll in pattern recognition receptor (PRR) against surface polysaccharide on microbes. We are investigating new aspects of lectins in cooperation with another PRR, toll-like receptor (TLR). In this study, we focus in the cooperation with SIGNR1 and TLR4 and revealed points as follows:
1)SIGNRl physically binds TLR2.
2)SIGNRl enhances TLR2/MD-2 oligomerization after stimulation with Gram-negative bacteria.
3)SIGNR1 recognizes non-reductive end of LPS core polysaccharide.
4)SINGR1 is a major receptor against model polysaccharide antigen dextran on resident peritoneal macrophages (rpMφ).
5)rpMφ enhances TN F-a production against S. typhimurium via SIGNR1.
6)Transfection of SIGNR1 improves TNF-a production form RAW264.7.
7)SIGNRl also binds TLR2.
8)RAW264.7 expressing SIGNR1 acquires Candicidal activity.
9)Soluble SIGNR1 binds hyphae form of C. albicans.
10)During infection to cells, SIGNR1 localizes at the invading sites of C. albicans.
These results suggest that SIGNR1 cooperates with TLR4 and TLR2 in response to Gram-negative bacteria and C. albicans, respectively, and plays roles in innate and acquired immunity. In addition, we generated new monoclonal antibody against another SIGNR family, SIGNR3. Using this antibody, we are investigating its expression pattern in vivo.
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