| Project/Area Number |
17390143
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Kyoto University |
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Principal Investigator |
IKUTA Koichi Kyoto University, Institute for Virus Research, Professor, ウイルス研究所, 教授 (90193177)
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| Co-Investigator(Kenkyū-buntansha) |
MAKI Kazushige Kyoto University, Institute for Virus Research, Lecture, ウイルス研究所, 講師 (10311424)
UEDA Masamichi Kyoto University, Institute for Virus Research, Assistant Professor, ウイルス研究所, 助手 (50115797)
HAYASHI Satoko Kyoto University, Institute for Virus Research, Research Associate, ウイルス研究所, 技術補佐員 (60402806)
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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 |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2006: ¥7,000,000 (Direct Cost: ¥7,000,000)
Fiscal Year 2005: ¥7,500,000 (Direct Cost: ¥7,500,000)
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| Keywords | T cell / interleukin / IL-7 / IL-7 receptor / dendritic cell / immune response / costimulatory molecule / IL-7レセプター |
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| Research Abstract |
The IL-7R α-chain (IL-7Rα) is the common receptor subunit for IL-7 and TSLP. It is reported that TSLP stimulates human dendritic cells (DC) to induce MHC class II molecule and various costimulatory molecules such as CD86. In this study we investigated the role of IL-7 and TSLP in differentiation, proliferation, and activation of mouse DC.
First, spleen and bone marrow DC expressed TSLPR and common γ chain (γc) at high levels, but IL-7Rα at low levels. DC induced by GM-CSF from bone marrow cells (BM-DC) expressed TSLPR and γc at high levels from early time points, but IL-7Rα at low levels only from late time points. In addition, IL-7Rα knockout (KO) mice had normal numbers of DC, and BM-DC were normally induced from IL-7Rα KO mice. Furthermore, IL-7 or TSLP had no effect on cell survival in isolated DC. These results suggested that IL-7 and TSLP are not essential for differentiation, proliferation, and survival of DC. Next, we analyzed the role of IL-7 and TSLP in activation of mouse DC. IL-7 induced MHC class II molecule on plasmacytoid DC (pDC) but not on conventional DC (cDC). On the other hand, TSLP induced CD86 on cDC but not on pDC. These results suggested the possibility that pDC and cDC differentially respond to IL-7 and TSLP. Thus, it was implicated that TSLP induces adaptive immune response by activating cDC and that IL-7 induces immune tolerance by activating pDC in the mouse.
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