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Antigen-mediated T cell expansion regulated by parallel pathways of death.

Authors
  • Ch'en, Irene L
  • Beisner, Daniel R
  • Degterev, Alexei
  • Lynch, Candace
  • Yuan, Junying
  • Hoffmann, Alexander
  • Hedrick, Stephen M
Type
Published Article
Journal
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Publication Date
Nov 11, 2008
Volume
105
Issue
45
Pages
17463–17468
Identifiers
DOI: 10.1073/pnas.0808043105
PMID: 18981423
Source
Medline
License
Unknown

Abstract

T cells enigmatically require caspase-8, an inducer of apoptosis, for antigen-driven expansion and effective antiviral responses, and yet the pathways responsible for this effect have been elusive. A defect in caspase-8 expression does not affect progression through the cell cycle but causes an abnormally high rate of cell death that is distinct from apoptosis and does not involve a loss of NFkappaB activation. Instead, antigen or mitogen activated Casp8-deficient T cells exhibit an alternative type of cell death similar to programmed necrosis that depends on receptor interacting protein (Ripk1). The selective genetic ablation of caspase-8, NFkappaB, and Ripk1, reveals two forms of cell death that can regulate virus-specific T cell expansion.

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