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

被引:64
作者
D'Cruz, Louise M. [1 ]
Rubinstein, Mark P. [1 ]
Goldrath, Ananda W. [1 ]
机构
[1] Univ Calif San Diego, Div Biol Sci, La Jolla, CA 92093 USA
基金
美国国家卫生研究院;
关键词
Infection; Pathogen; Transcription factor; Immune response; TRANSCRIPTIONAL REPRESSOR BLIMP-1; IL-7; RECEPTOR-ALPHA; LOOP-HELIX PROTEINS; CUTTING EDGE; IN-VIVO; HOMEOSTATIC PROLIFERATION; CLONAL EXPANSION; REGULATORS BIM; EXPRESSION; APOPTOSIS;
D O I
10.1016/j.smim.2009.02.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:92 / 98
页数:7
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