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2014 Fiscal Year Final Research Report

Role of SLC15A4 in controling lysosomal environment and inflammatory responses

Research Project

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Project/Area Number 25871165
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Immunology
Cell biology
Research InstitutionResearch Institute, International Medical Center of Japan

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)

Research Collaborator DEMOTO Shiho  
SHIMIZU Yukiko  
TANAKA Kaori (FURUYAMA Kaori)  
YOSHIDA Reiko (SUGITANI Reiko)  
KARIU Hitomi  
Project Period (FY) 2013-04-01 – 2015-03-31
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
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.

Free Research Field

免疫学

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Published: 2016-06-03  

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