Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 May 9;10:2123. doi: 10.1038/s41467-019-10015-4

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 5 — Immunological consequences of changes in nutrient signalling. Activation of AMP-activated protein kinase (AMPK) or inhibition of mammalian Target of Rapamycin Complex 1 (mTORC1) signalling promotes the differentiation of regulatory T (T_Reg) cells over effector T cell subsets (T_E), inhibits natural killer (NK) cell functions, and increases the proinflammatory outputs of dendritic cells (DC). Loss of cMyc expression inhibits the functions of T_E subsets and NK cells. Activation of general control nonderepressible 2 (GCN2) signalling promotes T_Reg differentiation, inhibits Th17 differentiation, inhibits CD8 T cell function, and enhances the function of DC. Kynurenine (Kyn)-mediated aryl hydrocarbon receptor (AhR) signalling promotes the differentiation of T_Reg