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lüll Surviving the crash: transitioning from effector to memory CD8+ T cell D'Cruz LM; Rubinstein MP; Goldrath AWSemin Immunol 2009[Apr]; 21 (2): 92-8One 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.|*Cytotoxicity, Immunologic[MESH]|*Immunologic Memory[MESH]|Animals[MESH]|Apoptosis[MESH]|CD8-Positive T-Lymphocytes/immunology/*metabolism/pathology[MESH]|Cell Differentiation[MESH]|Cytokines/genetics/immunology/metabolism[MESH]|DNA-Binding Proteins/immunology[MESH]|Humans[MESH]|Infections/*immunology[MESH]|Inhibitor of Differentiation Protein 2/immunology[MESH]|Positive Regulatory Domain I-Binding Factor 1[MESH]|Proto-Oncogene Proteins c-bcl-6[MESH]|Repressor Proteins/immunology[MESH]|Signal Transduction[MESH]|T-Box Domain Proteins/immunology[MESH]|T-bet Transcription Factor[MESH]|Transcriptional Activation/*immunology[MESH] |