Surviving the crash: transitioning from effector to memory CD8+ T cell

One outcome of infection is the formation of long-lived immunological memory, which provides durable protection from symptomatic re-infection. In response to infection or vaccination, T cells undergo dramatic proliferation and differentiate into effector T cells that mediate removal of the pathogen. Following pathogen clearance, the majority of effector cells die, restoring lymphocyte homeostasis. However, a small number of antigen-specific cells survive and seed the memory T cell population. Here, we focus on recent advances in identifying the key proteins and transcription factors that allow a portion of effector CD8(+) T cells to persist after contraction of the immune response, forming a memory cell population programmed for long-term self-renewal and survival. We also examine new findings addressing the role of environmental cues such as cytokines and co-stimulatory molecules in CD8(+) memory T cell formation and how the cell-extrinsic cues influence the molecular players of intracellular pathways important for memory formation.