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. 2017 Feb 24;8(3):88. doi: 10.3390/genes8030088

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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MYC-dependent metabolic reprograming in immunity As schematically shown here, MYC regulates immune cell metabolic reprogramming in different contexts. Colony-stimulating factor-1 (CSF-1) induces MYC expression and engages glycolysis and glutaminolysis that are required for driving macrophage proliferation. Maturation of DCs relies oxidative phosphorylation (OXPHOS) and is associated with Interferon (IFN) mediated MYCL upregulation. MYC is a component of the T cell receptor (TCR) mediated transcriptional network in T cells and coordinately controls glycolysis, pentose phosphate pathway (PPP) and glutaminolysis to support proliferation and differentiation following T cell activation. Upon BCR stimulation, upregulated MYC drives glycolysis, glutaminolysis and OXPHOS to support B cell growth and proliferation. MΦ: Macrophages; DC: Dendritic cells; BCR: B cell receptor.