Journal
INOSITOL PHOSPHOLIPID SIGNALING IN PHYSIOLOGY AND DISEASE
Volume 1280, Issue -, Pages 30-34Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.12059
Keywords
PI3K; Th17; mTOR; HIF-1
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Funding
- Japan Society for the Promotion of Science [21790476]
- Takeda Science Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Ministry of Health, Labour and Welfare, Japan [20060021]
- National Grant-in-Aid for the Establishment of a High-Tech Research Center in a Private University
- Ministry of Education, Culture, Sports, Science and Technology, Japan
- Grants-in-Aid for Scientific Research [20060021, 21790476, 24790479] Funding Source: KAKEN
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Interleukin (IL)-17-producing helper T (Th17) cells serve as a Th subset involved in epithelial cell-and neutrophil-mediated immune responses against extracellular microbes and in the development of various autoimmune diseases. The differentiation of Th17 cells is controlled by a number of intracellular signaling cascades and a complex network of transcription factors. Recently, it has been shown that PI3K, Akt, and mammalian target of rapamycin (mTOR) complexes, such as mTORC1 and mTORC2, also positively regulate Th17 differentiation both in vivo and in vitro via multiple mechanisms; here, we review the current knowledge regarding the mechanisms through which these molecules enhance Th17 differentiation.
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