IL2 and viral infectious disease: Due to expression of both CD122 and CD132 receptors involved in cytokine signaling, memory T cells also gain the ability to be activated in the absence of T cell receptor (TCR) triggering and by IL-2 or IL-15 cytokine signaling alone, bypassing the need for TCR engagement in a process called “bystander activation.” This antigen-nonspecific activation can be induced during inflammatory conditions, which is dependent on strong stimuli,such as acute viral infections or cancer immunostimulatory therapies, to maintain function and survival (2–4).