4.7 Article Proceedings Paper

Role of PI3K/Akt and mTOR complexes in Th17 cell differentiation

出版社

BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.12059

关键词

PI3K; Th17; mTOR; HIF-1

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资金

  1. Japan Society for the Promotion of Science [21790476]
  2. Takeda Science Foundation
  3. Mochida Memorial Foundation for Medical and Pharmaceutical Research
  4. Ministry of Health, Labour and Welfare, Japan [20060021]
  5. National Grant-in-Aid for the Establishment of a High-Tech Research Center in a Private University
  6. Ministry of Education, Culture, Sports, Science and Technology, Japan
  7. Grants-in-Aid for Scientific Research [20060021, 21790476, 24790479] Funding Source: KAKEN

向作者/读者索取更多资源

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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