De novo fatty acid synthesis controls the fate between regulatory T and T helper 17 cells

By L. Berod, Christin Friedrich, A. Nandan, J. Freitag, S. Hagemann, Kirsten Harmrolfs, Aline Sandouk, C. Hesse, C. N. Castro, H. Bähre and 10 more. Nature Medicine, 2014

851 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/54d6029667194835d46efd6a50b03b78acbb35ed

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Citations in the corpus

The Balance of Th17 versus Treg Cells in Autoimmunity (2018, background): “Th17 cells rely on acetyl-CoA carboxylase 1-mediated de novo fatty acid synthesis and the underlying glycolytic–lipogenic metabolic pathway for their differentiation [77].”
Unraveling the Complex Interplay Between T Cell Metabolism and Function (2018, background): “Consistent with the role of FAS in Th17 cells, T cell–specific deletion of ACC1 protects mice from EAE, coincidentally reducing the number of IFN-γ-producing Th17 cells and increasing the number of Foxp3+ Treg cells in the spinal cord (119).”
T cell metabolism drives immunity (2015, background): “Although activated T cells readily acquire and use extracellular fatty acids, it appears that there may also be cell-intrinsic requirements for de novo–synthesized fatty acids (Berod et al., 2014; Lee et al., 2014; O’Sullivan and Pearce, 2014; O’Sullivan et al., 2014).”
Mitochondrial metabolism and cancer (2017, background): “CTLs and helper T cells responding to antigenic stimulation engage in a proliferative response that – similar to cancer cell proliferation – extensively relies on glycolysis and is supported by mitochondrial fragmentation [207-209].”
Metabolic Instruction of Immunity (2017, positive): “, 2007), and pharmacological inhibition of de novo fatty acid synthesis prevents Th17 differentiation and instead enforces a Treg cell phenotype (Berod et al., 2014).”
Mitochondria in the regulation of innate and adaptive immunity (2015, positive): “Pharmacologic and genetic inhibition of the enzyme acetyl-CoA carboxylase 1 (ACC1), the enzyme that catalyzes the first step of de novo fatty-acid synthesis, impaired Th17 cell differentiation, and promoted Tregs in vitro and in vivo, as well as attenuated EAE in mice (Berod et al., 2014).”