Metabolic Pathways In Immune Cell Activation And Quiescence

By Erika L. Pearce, Edward J. Pearce. Immunity, 2013

1,542 citations recorded by the source corpus.

Studies of immune system metabolism (“immunometabolism”) segregate along two paths. The first investigates the effects of immune cells on organs that regulate whole body metabolism, such as adipose tissue and liver. The second explores the role of metabolic pathways within immune cells and how this regulates immune response outcome. Distinct metabolic pathways diverge and converge at many levels and cells therefore face choices in how to achieve their metabolic goals. There is interest in fully understanding how and why immune cells commit to particular metabolic fates, and in elucidating the immunologic consequences of reaching a metabolic endpoint by one pathway versus another. This is particularly intriguing since metabolic commitment is influenced not only by substrate availability, but also by signaling pathways elicited by metabolites. Thus metabolic choices in cells enforce fate and function and this area will be the subject of this review.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/4c49e925f9f0b1347d2ef2e0a8142262630f53d6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

In Immunology

Citations in the corpus

Immunometabolism governs dendritic cell and macrophage function (2016, background): “This area is reviewed extensively elsewhere (Odegaard and Chawla, 2011; Pearce and Pearce, 2013; Galván-Peña and O’Neill, 2014).”
T Cell Dysfunction in Cancer (2018, background): “Whereas naive T cells largely rely on oxidative phosphorylation (OXPHOS), they switch to the use of aerobic glycolysis upon antigen stimulation, to generate the required ATP (Chang et al., 2013; Pearce and Pearce, 2013).”
Distinct Signaling of Coreceptors Regulates Specific Metabolism Pathways and Impacts Memory Development in CAR T Cells. (2016, background): “Activation is associated with a biosynthetic and bioenergetics flux required to support T cell proliferation and function (Pearce and Pearce, 2013; Wang and Green, 2012).”
Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “Additionally, recent work highlights the importance of metabolic changes during activation of macrophages and dendritic cells (34, 35).”
Microglial M1/M2 polarization and metabolic states (2016, background): “…data on the bioenergetics of polarization states has been generated in peripheral immune cells (Biswas and Mantovani, 2012; O’Neill and Hardie, 2013; Pearce and Pearce, 2013) with only a few studies examining microglia (Moss and Bates, 2001; Chenais et al., 2002; Bernhart et al., 2010; Sohn et…”
Dengue and severe dengue (2025, positive): “Likewise, as metabolism regulates immune cell function (178, 179), polymorphisms in oxysterol binding protein-like 10 ( OSBPL10 ) and retinoid x receptor alpha ( RXRA ) genes may explain the reduced susceptibility of those of African descent to severe dengue (180).”
The energy sensor AMPK regulates T cell metabolic adaptation and effector responses in vivo. (2015, background): “SRC represents increased mitochondrial electrochemical potential, which can be used to generate ATP, and is a key index of T cell metabolic fitness (Pearce and Pearce, 2013; van der Windt et al., 2012).”
Mitochondria in the regulation of innate and adaptive immunity (2015, positive): “Predictably, this conversion requires a shift in cellular metabolism from a catabolic to an anabolic metabolic program (Pearce and Pearce, 2013).”
TLR-driven early glycolytic reprogramming via the kinases TBK1-IKKε supports the anabolic demands of dendritic cell activation (2014, methodology): “Although we found contributions of signaling via PI(3)K and mTOR to the phosphorylation of Akt, we identified TBK1-IKKε as the most important kinases in regulating the phosphorylation and activation of Akt after stimulation with LPS.”
T cell lipid peroxidation induces ferroptosis and prevents immunity to infection (2015, background): “TCR stimulation has been shown to induce production of discrete species of ROS (i.e., hydrogen peroxide and superoxide anion), involving a phagocyte type NADPH oxidase expressed by T cells and the FAS pathway (Devadas et al., of bacteria, whereas groups of mice undergoing primary infection were all ”
Inhibiting glycolytic metabolism enhances CD8+ T cell memory and antitumor function. (2013, positive): “Similar to Tns, memory CD8 + T cells use FAO to meet their energy demands (19, 20).”