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mTOR Signaling pathway as a master regulator of memory CD8+ T‐cells, Th17, and NK cells development and their functional properties.

Authors :
Rostamzadeh, Davood
Yousefi, Mehdi
Haghshenas, Mohammad Reza
Ahmadi, Majid
Dolati, Sanam
Babaloo, Zohreh
Source :
Journal of Cellular Physiology. Aug2019, Vol. 234 Issue 8, p12353-12368. 16p.
Publication Year :
2019

Abstract

The mammalian target of rapamycin (mTOR) is a member of the evolutionary phosphatidylinositol kinase‐related kinases (PIKKs). mTOR plays a pivotal role in the regulation of diverse aspects of cellular physiology such as body metabolism, cell growth, protein synthesis, cell size, autophagy, and cell differentiation. Immunologically, mTOR has a fundamental part in controlling and shaping diverse functions of innate and adaptive immune cells, in particular, T‐cell subsets differentiation, survival, and metabolic reprogramming to ultimately regulate the fate of diverse immune cell types. Researchers report that rapamycin, a selective mTOR inhibitor, and immunosuppressive agent, has surprising immunostimulatory effects on inducing both quantitative and qualitative aspects of virus‐specific memory CD8+ T‐cells differentiation and homeostasis in a T‐cell‐intrinsic manner. The mTOR signaling pathway also plays a critical role in dictating the outcome of regulatory T cells (Treg), T helper 17 (Th17) cells, and natural killer (NK) cells proliferation and maturation, as well as the effector functions and cytotoxic properties of NK cells. Manipulation of mTOR activity is a critical therapeutic approach for pharmacological agents that seek to inhibit mTOR. This approach should enhance specific memory CD8 + T‐cells responses and induce fully functional effector properties of NK cells to provoke their antitumor and antiviral activities. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00219541
Volume :
234
Issue :
8
Database :
Academic Search Index
Journal :
Journal of Cellular Physiology
Publication Type :
Academic Journal
Accession number :
135977184
Full Text :
https://doi.org/10.1002/jcp.28042