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. 2012 Sep;249(1):5-13.
doi: 10.1111/j.1600-065X.2012.01158.x.

Metabolism and autophagy in the immune system: immunometabolism comes of age

Jeffrey C Rathmell  1
Affiliations

Metabolism and autophagy in the immune system: immunometabolism comes of age

Jeffrey C Rathmell. Immunol Rev. 2012 Sep.
No abstract available

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Conflict of interest statement

The author has no conflicts of interest to declare.

Figures

Fig. 1
Fig. 1. Links between metabolism and immunity
Resting lymphocytes use an oxidative metabolism for maximal energy generation. Upon stimulation, the Akt/mammalian target of rapamycin (mTOR), c-Myc, and estrogen related receptor-α pathways promote effector T cells to switch to a glycolytic metabolism that promotes cell growth for rapid proliferation. Classical M1 macrophages are also highly glycolytic and inflammatory. If AMP-activated protein kinase is stimulated, however, to suppress mTOR and promote lipid oxidation, regulatory T cells (Tregs) are favored. Suppressive M2 macrophages are also oxidative. Autophagy, apoptosis, and necroptosis pathways can also be metabolically regulated and can shape the immune response. Lymphocytes and macrophages are also closely tuned to adipose tissue through lipid signaling mechanisms and adipokines. T cells and macrophages then can play key roles to regulate insulin resistance and the metabolic syndrome.
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