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Metabolic programming in immune cells is a critical determinant of their downstream functions and mounting a robust immune response is energetically expensive. Increased glycolysis is generally associated with elevated proinflammatory activity, whereas fatty acid oxidation and oxidative phosphorylation is associated with quiescence and anti-inflammatory functions [104]. At the population level, a balance between these programs allows for proinflammatory immune-mediated pathogen clearance, while preserving tissue repair functions and long-lived immunity in the case of adaptive immune cells. In addition to the importance of overall metabolic programming, specific metabolites such as succinate, itaconate, and β-hydroxybutyrate regulate immune cell function [105, 106]. Therefore, targeting immune cell metabolism represents an attractive strategy for modulating immune responsiveness and vaccine efficacy. It should be noted that the simplified model presented here is derived from mostly in vitro studies and whether this programming balance occurs in vivo or is maintained during aging is not known. Future studies are needed to test whether basal metabolic programming and/or activation-induced metabolic upregulation in innate immune cells is retained during aging and what cues stimulate this reprogramming.