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Role of PI3K/Akt and mTOR complexes in Th17 cell differentiation
Author(s) -
Nagai Shigenori,
Kurebayashi Yutaka,
Koyasu Shigeo
Publication year - 2013
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12059
Subject(s) - mtorc2 , mtorc1 , pi3k/akt/mtor pathway , microbiology and biotechnology , protein kinase b , transcription factor , cellular differentiation , immune system , intracellular , chemistry , biology , signal transduction , cancer research , immunology , gene , biochemistry
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.