| Project/Area Number |
25871165
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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 |
Immunology
Cell biology
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| Research Institution | Research Institute, International Medical Center of Japan |
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Principal Investigator |
KOBAYASHI Toshihiko 独立行政法人国立国際医療研究センター, その他部局等, その他 (40613203)
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| Research Collaborator |
DEMOTO Shiho
SHIMIZU Yukiko
TANAKA Kaori (FURUYAMA Kaori)
YOSHIDA Reiko (SUGITANI Reiko)
KARIU Hitomi
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 自然免疫の炎症応答制御機構 / ライソゾーム / アミノ酸輸送 / TLR / 自己免疫疾患 / 自然免疫 / B細胞 / トランスポーター / 炎症制御 / mTOR / ライソゾーム環境調節 / 自然免疫応答 / 自己抗体産生 |
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| Outline of Final Research Achievements |
Immune cells have a unique regulation system of endo/lysosomes to harness their inflammatory signaling that results in secretion of mediators or cytokines. Our project aimed to reveal the molecular mechanism how the inflammatory response that takes place in the lysosome, such as Toll-like receptor (TLR) signaling, is controlled by SLC15A4, a lysosome-resident amino acid transporter. We found the novel mechanism that SLC15A4 regulates the activity of mTOR complex that is essential for the type I interferon signaling triggered by TLR7 or TLR9. We also found that this regulatory mechanism played a key role in production of pathogenic autoantibodies in the autoimmune disease model. Our finding suggested that SLC15A4 could be a therapeutic target of inflammatory diseases.
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