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dc.contributor.authorCh'en, Irene L.
dc.contributor.authorBeisner, Daniel R.
dc.contributor.authorDegterev, Alexei
dc.contributor.authorLynch, Candace
dc.contributor.authorYuan, Junying
dc.contributor.authorHoffmann, Alexander
dc.contributor.authorHedrick, Stephen M.
dc.date.accessioned2019-10-05T16:04:40Z
dc.date.issued2008
dc.identifier.citationCh’en, I. L., D. R. Beisner, A. Degterev, C. Lynch, J. Yuan, A. Hoffmann, and S. M. Hedrick. 2008. “Antigen-Mediated T Cell Expansion Regulated by Parallel Pathways of Death.” Proceedings of the National Academy of Sciences 105 (45): 17463–68. https://doi.org/10.1073/pnas.0808043105.
dc.identifier.issn0027-8424
dc.identifier.issn0744-2831
dc.identifier.issn1091-6490
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41483459*
dc.description.abstractT 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 NF kappa B 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, NF kappa B, and Ripk1, reveals two forms of cell death that can regulate virus-specific T cell expansion.
dc.language.isoen_US
dc.publisherNational Academy of Sciences
dash.licenseLAA
dc.titleAntigen-mediated T cell expansion regulated by parallel pathways of death
dc.typeJournal Article
dc.description.versionVersion of Record
dc.relation.journalProceedings of the National Academy of Sciences of the United States of America
dash.depositing.authorYuan, Junying::c7e832b918fc7c2356d6c49fe1a0b135::600
dc.date.available2019-10-05T16:04:40Z
dash.workflow.comments1Science Serial ID 90181
dc.identifier.doi10.1073/pnas.0808043105
dash.source.volume105;45
dash.source.page17463


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