4.5 Review

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

Journal

SEMINARS IN IMMUNOLOGY
Volume 21, Issue 2, Pages 92-98

Publisher

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2009.02.002

Keywords

Infection; Pathogen; Transcription factor; Immune response

Categories

Funding

  1. Cancer Research Institute
  2. Pew Scholar Award
  3. California Breast Cancer Research Program Award
  4. National Institutes of Health
  5. Leukemia and Lymphoma Career Development Fellowship
  6. Prevent Cancer Foundation

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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.

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