The CD28 signaling pathway regulates glucose metabolism.

By Kenneth A. Frauwirth, J. Riley, Marian H. Harris, R. Parry, J. Rathmell, D. Plas, R. Elstrom, C. June, Craig B. Thompson. Immunity, 2002

1,419 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/afc793156b1d5e6932d4ca6cf7e89422afcd6236

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Citations in the corpus

T-lymphocyte activation (2005, positive): “Recently it has been reported that Akt/PKB links the costimulatory molecule CD28 to the control of cellular glucose metabolism (Frauwirth et al., 2002).”
Mitochondrial Respiratory Capacity Is A Critical Regulator Of CD8+ T Cell Memory Development (2011, background): “Consistent with the idea that proliferating T cells use glycolysis for energy (Frauwirth et al., 2002; Jones and Thompson, 2007), we found that IL-2 Teff cells displayed high basal ECAR (Figure 1D) when compared to IL-15 memory T cells.”
The Glucose Transporter Glut1 is Selectively Essential for CD4 T Cell Activation and Effector Function (2014, positive): “In vitro-stimulated murine and human T cells express high levels of Glut1 (Slc2a1) (Frauwirth et al., 2002; Jacobs et al., 2008), and Teff cells maintain levels of Glut1 higher than those of Treg (Michalek et al., 2011a).”
The Principles of Engineering Immune Cells to Treat Cancer (2017, background): “In natural T cells, glutamine and glucose import are CD28 dependent (Carr et al., 2010; Frauwirth et al., 2002).”
Metabolic Regulation of Immune Responses (2014, background): “As reported previously, T cell proliferation and survival was dependent on glycolysis when cells were cultured in medium containing glucose and glutamine (86, 91, 96, 98).”
Inhibiting glycolytic metabolism enhances CD8+ T cell memory and antitumor function. (2013, neutral): “After antigen encounter, however, T cells shift to glycolytic metabolism to sustain effector function (15–18).”
SHP-1 and SHP-2 Associate with Immunoreceptor Tyrosine-Based Switch Motif of Programmed Death 1 upon Primary Human T Cell Stimulation, but Only Receptor Ligation Prevents T Cell Activation1 (2004, methodology): “Interaction of the GST-CD150 cytoplasmic tail and SH2D1A was determined by precipitation of immune complexes using glutathione-coupled agarose beads, followed by Western blotting, as previously described (30).”
Metabolic Regulation of T Lymphocytes (2013, background): “In the case of CTLA-4, ligation of this receptor has been shown to terminate PI3K/Akt signaling (107), thereby diminishing glucose metabolism that is required for optimal cell growth and function (23, 54).”
T Cell Dysfunction in Cancer (2018, background): “For instance, the inhibitory receptor CTLA-4 on T cells competes with CD28 for B7 ligands and thereby suppresses the CD28-mediated T cell costimulation that is essential to increase T cell glucose uptake and metabolism (Frauwirth et al., 2002; Parry et al., 2005).”
Complex N-glycan number and degree of branching cooperate to regulate cell proliferation and differentiation. (2007, background): “TCR signaling induces large increases in glucose uptake (Frauwirth et al., 2002) and Mgat5 gene expression (Morgan et al., 2004) as well as UDP-GlcNAc, surface b1,6GlcNAc-branched N-glycans, and, finally, CTLA-4 (Figure 6E).”
The energy sensor AMPK regulates T cell metabolic adaptation and effector responses in vivo. (2015, background): “Upon activation, naive T cells shift to- ward a pro-growth metabolic program characterized by increased glucose and amino acid metabolism (Carr et al., 2010; Frauwirth et al., 2002; Nakaya et al., 2014; Sinclair et al., 2013; Wang et al., 2011).”
Aerobic glycolysis promotes T helper 1 cell differentiation through an epigenetic mechanism (2016, background): “A metabolic hallmark of activated T cells is aerobic glycolysis (5), the conversion of glucose to lactate in the presence of oxygen, but its physiopathological functions remain incompletely understood (6–8).”
PD-1 signaling in primary T cells (2009, background): “While T-cell receptor (TCR) engagement orchestrates the changes in the T-cell gene expression profile, which enable a T cell to transform from perhaps the most quiescent cell in the body to an actively expanding immune effector (36, 37), TCR engagement does not instruct T cells to uptake the necessa”
CTLA-4 and PD-1 Receptors Inhibit T-Cell Activation by Distinct Mechanisms (2004, background): “CTLA-4 ligation inhibits this increase in glucose metabolism (26), and we were interested in determining if PD-1 engagement also targeted the ability of T cells to import and utilize nutrients.”