The activation of naive T cells does not complete their maturation process; instead, it is the starting point for the changes that result in T-cell-mediated immunity. At the initiation of an infection, individual antigen-specific T cells become activated and expand robustly to combat the pathogen. As the pathogen is eradicated, the large population of activated T cells must contract dramatically to ensure homeostasis of the immune system. However, a discrete but small population of antigen-specific T cells persists. These long-lived T cells have properties distinct from naive or activated T cells, including self-renewal through homeostatic proliferation and the ability to rapidly proliferate and regain effector function upon re-exposure to antigen. These are the cardinal features of cell-mediated immunologic memory.

Immunologic memory refers to the observation that after an initial exposure and mounting of an effective immune response to a pathogen, subsequent interactions with that pathogen elicit rapid and robust T-cell activation, with more efficient clearance of the pathogen. Memory is the foundation of vaccination because immunization with pathogen-specific antigens induces a memory response so that first exposure of the host to the intact pathogen results in a rapid, effective response, thus abrogating signs and symptoms of the infection.

Within days of infection, subsets of activated effector CD8+ T cells can be identified with different cell fates: those that are terminally differentiated and those that have the potential to develop into memory cells. Single-cell adoptive transfer experiments demonstrate that individual naive CD8+ T cells have the ability to differentiate into a heterogeneous pool of short-lived effector and long-lived memory cells, likely in response to differences in antigen specificity and duration of stimulation, precursor frequency, and the inflammatory environment.

Different subsets of memory cells are observed after resolution of infection. The two main classes are effector memory and central memory T cells. Effector memory T cells, characterized by lack of expression of LN homing molecules CD62L and CCR7, rapidly produce cytokines in response to restimulation with previously encountered antigen, thereby allowing for rapid responses to invading pathogens. These cells preferentially reside in the circulation. In contrast, central memory cells express high levels of CD62L and CCR7, are more prevalent in lymphoid tissues, and mount a robust proliferative response after reencountering antigen and are longer-lived. More recently, tissue-resident memory cells have been identified. These tissue-resident memory cells have been identified in the lungs, skin, liver, and the female reproductive tract. They are characterized by expression of the integrin CD103, which aids in tissue entry, and CD69, which promotes tissue retention.

As with differentiation of naive T cells into efficient effectors, cytokines play an important role in memory T-cell development and maintenance. IL-2 is essential for initial memory cell differentiation, whereas IL-7 and IL-15 are crucial for memory cell persistence. Other signals, such as the strength of antigenic and inflammatory signals during T-cell activation, also influence memory cell development and maintenance. An important consideration for memory development is cell–cell interactions because CD4+ T cells are required during initial priming of CD8+ cells for development of fully functional CD8+ memory cells. A number of infectious disease models have demonstrated that in the absence of CD4+ T-cell help, fewer CD8+ memory T cells are maintained, and those that do persist are of the central memory phenotype.

Although great progress has been made in elucidating the molecular underpinnings of immunologic memory, much remains to be learned. Recent data have emerged on the importance of the cellular metabolic state in the control of memory T-cell differentiation. As CD8+ T cells are activated, they transition from using primarily oxidative phosphorylation to generate basal energy in the quiescent state to using glycolysis during the effector phase and then back to using oxidative phosphorylation as memory cells. In experimental models, manipulations of the cell’s metabolic profile can influence effector function and memory differentiation. As additional discoveries are made, it is anticipated that new approaches will develop to improve T-cell responses to vaccines against infectious agents, to promote T-cell recall responses to pathogens that today result in chronic infections, and to harness host T-cell responses to combat tumors.

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