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The determinants of protective CD8+ memory T cell (CD8+TM) immunity remain incompletely defined and may in fact constitute an evolving agency as aging CD8+TM progressively acquire enhanced rather than impaired recall capacities. Here, we show that old as compared to young antiviral CD8+TM more effectively harness disparate molecular processes (cytokine signaling, trafficking, effector functions, and co-stimulation/inhibition) that in concert confer greater secondary reactivity. The relative reliance on these pathways is contingent on the nature of the secondary challenge (greater for chronic than acute viral infections) and over time, aging CD8+TM re-establish a dependence on the same accessory signals required for effective priming of naïve CD8+T cells in the first place. Thus, our findings reveal a temporal regulation of complementary recall response determinants that is consistent with the recently proposed “rebound model” according to which aging CD8+TM properties are gradually aligned with those of naïve CD8+T cells; our identification of a broadly diversified collection of immunomodulatory targets may further provide a foundation for the potential therapeutic “tuning” of CD8+TM immunity., Author summary Immune protection provided by antiviral memory T cells relies in part on their capacity for prodigious proliferative expansion in the context of a re-infection, a proficiency that, perhaps surprisingly, is augmented rather than curtailed as memory T cells progress with age. In the present work, which draws on emerging evidence that T cell memory is not a stable trait but a progressively evolving property, we have begun to elucidate the mechanistic foundations for this age-associated amplification of memory T cell recall potential. Altogether, aged in comparison to young memory T cells more effectively engage multiple distinct stimulatory pathways and better eschew restraints exercised by inhibitory interactions. In this regard aged memory T cells resemble naïve T cells that depend on much of the same accessory signals to mount potent primary T cell responses. Our findings therefore provide further support for the “rebound model” of memory T cell maturation according to which aging memory T cell properties are progressively aligned with those of naïve T cells; they reveal a fundamentally temporal contingency of recall responses on the integrated activity of highly diversified molecular cues; and they identify a set of disparate targets for potential T cell-focused therapeutic interventions.