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. 2022 Apr 19;219(6):e20211314. doi: 10.1084/jem.20211314

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© 2022 Chen et al.

This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

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Figure 3. — CD36 mediates differential responses in T cell subsets. (A) In T_reg cells, CD36 is upregulated in the TME and facilitates fatty acid (FA) uptake, which subsequently stimulates PPAR-β signaling. Both CD36-mediated fatty acid uptake and PPAR-β signaling support mitochondrial OXPHOS. As a consequence, NAD⁺ is continuously produced from nicotinamide adenine dinucleotide (NADH) through the mitochondrial electron transport chain (ETC). T_reg cells utilize this NAD⁺ pool for metabolism of L-lactate to pyruvate so that they are better adapted to a high-lactate TME and maintain viability and immunosuppressive functions. (B) In TME CD8⁺ T cells, CD36-mediated fatty acid uptake leads to lipid peroxidation and ferroptosis so that these cells are not able to produce cytotoxic cytokines.