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St Paul, Michael; Saibil, Samuel D; Han, SeongJun; Israni-Winger, Kavita; Lien, Scott C; Laister, Rob C; Sayad, Azin; Penny, Susanne; Amaria, Rodabe N; Haydu, Lauren E; Garcia-Batres, Carlos R; Kates, Meghan; Mulder, David T; Robert-Tissot, Céline; Gold, Matthew J; Tran, Charles W; Elford, Alisha R; Nguyen, Linh T; Pugh, Trevor J; Pinto, Devanand M; Wargo, Jennifer A; Ohashi, Pamela S
Cell metabolism, 12/2021, Letnik: 33, Številka: 12Journal Article
Metabolic programming is intricately linked to the anti-tumor properties of T cells. To study the metabolic pathways associated with increased anti-tumor T cell function, we utilized a metabolomics approach to characterize three different CD8 T cell subsets with varying degrees of anti-tumor activity in murine models, of which IL-22-producing Tc22 cells displayed the most robust anti-tumor activity. Tc22s demonstrated upregulation of the pantothenate/coenzyme A (CoA) pathway and a requirement for oxidative phosphorylation (OXPHOS) for differentiation. Exogenous administration of CoA reprogrammed T cells to increase OXPHOS and adopt the CD8 Tc22 phenotype independent of polarizing conditions via the transcription factors HIF-1α and the aryl hydrocarbon receptor (AhR). In murine tumor models, treatment of mice with the CoA precursor pantothenate enhanced the efficacy of anti-PDL1 antibody therapy. In patients with melanoma, pre-treatment plasma pantothenic acid levels were positively correlated with the response to anti-PD1 therapy. Collectively, our data demonstrate that pantothenate and its metabolite CoA drive T cell polarization, bioenergetics, and anti-tumor immunity.
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in: SICRIS
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