Abstract
Novel therapies targeting immune checkpoint molecules have redefined the treatment of cancer at advanced stages and brought hope to millions of patients worldwide. Monoclonal antibodies targeting immune-inhibitory receptors often lead to complete and objective responses as well as to durable progression-free survival where all other therapeutic approaches fail. Yet, many tumors show significant resistance to checkpoint blockade through mechanisms that are only starting to come to light. An alluring alternative strategy to reinvigorate anticancer immune responses comes from the emerging field of immuno-metabolism. Over the past few years, numerous studies revealed that many well-known metabolic playmakers also serve as critical checkpoints in immune homeostasis and immunity against tumors. Here, we survey recent insights into the intimate and intertwining links between T cell metabolic programs and environmental cues in the tumor milieu. Transferring these new findings from the bench to the bedside may soon entirely re-shape the field of cancer immunotherapy and significantly improve the lives of patients.
Highlights
Immunotherapy has become a paradigm-shifting approach showing unmatched efficacy in patients with advanced malignancies
Glut1 expression promoted Treg expansion, it reduced their suppressive activity and Foxp3 expression. This indicates that Treg cells might occasionally switch to aerobic glycolysis and expand when they receive inflammatory signals, and subsequently switch back to FAO and oxidative phosphorylation (OXPHOS) to achieve maximal suppressive potency
Kishore et al [21] have studied the metabolic needs for migratory Treg. They demonstrated that glycolysis strongly promotes Treg migration and is triggered by a PI3K–mTORC2-mediated pathway driving the activation of the enzyme glucokinase
Summary
Immunotherapy has become a paradigm-shifting approach showing unmatched efficacy in patients with advanced malignancies. The success of these treatments is often limited to minor cohorts of patients. This calls for the development of alternative strategies for reinvigorating anticancer immunity. Pathways controlling T cell responses to external challenges often converge on the same limited set of enzymes, transcription factors, and signaling complexes serving as metabolic checkpoints [7, 8]. This highlights the elegant simplicity and dazzling complexity of T cell biology
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