ArticlePloS one2010
Caspase-3 is transiently activated without cell death during early antigen driven expansion of CD8(+) T cells in vivo.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
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- Ammonia-induced lysosomal and mitochondrial damage causes cell death of effector CD8Nature cell biology · 2024Article
- Oncogenic Fatty Acid Metabolism Rewires Energy Supply Chain in Gastric Carcinogenesis.Gastroenterology · 2024Article
- XIAP promotes the expansion and limits the contraction of CD8 T cell response through cell extrinsic and intrinsic mechanisms respectively.PLoS pathogens · 2023Article
- Paradoxical roles of caspase-3 in regulating cell survival, proliferation, and tumorigenesis.The Journal of cell biology · 2022Review
- MET Inhibition Sensitizes Rhabdomyosarcoma Cells to NOTCH Signaling Suppression.Frontiers in oncology · 2022Article
- Interleukin-1 blockade attenuates white matter inflammation and oligodendrocyte loss after progressive systemic lipopolysaccharide exposure in near-term fetal sheep.Journal of neuroinflammation · 2021Article
- Mutagenic Consequences of Sublethal Cell Death Signaling.International journal of molecular sciences · 2021Review
- Human umbilical cord mesenchymal stromal cells as an adjunct therapy with therapeutic hypothermia in a piglet model of perinatal asphyxia.Cytotherapy · 2021Article
- Effects of prenatal synthetic cannabinoid exposure on the cerebellum of adolescent rat offspring.Heliyon · 2021Article
- Galectin-9 interacts with PD-1 and TIM-3 to regulate T cell death and is a target for cancer immunotherapy.Nature communications · 2021Article
- Oxidized Low-Density Lipoprotein Induces Macrophage Production of Prothrombotic Microparticles.Journal of the American Heart Association · 2020Article
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- The novel cyclophilin-D-interacting protein FASTKD1 protects cells against oxidative stress-induced cell death.American journal of physiology. Cell physiology · 2019Article
- Caspase-8 restricts antiviral CD8 T cell hyperaccumulation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Acute LPS sensitization and continuous infusion exacerbates hypoxic brain injury in a piglet model of neonatal encephalopathy.Scientific reports · 2019Article
- The PD-1/PD-L1 Pathway Affects the Expansion and Function of Cytotoxic CD8Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCD8(+) T cell responses develop rapidly during infection and are swiftly reduced during contraction, wherein >90% of primed CD8(+) T cells are eliminated. The role of apoptotic mechanisms in controlling this rapid proliferation and contraction of CD8(+) T cells remains unclear. Surprisingly, evidence has shown non-apoptotic activation of caspase-3 to occur during in vitro T-cell proliferation, but the relevance of these mechanisms to in vivo CD8(+) T cell responses has yet to be examined. METHODS AND
findingsWe have evaluated the activity of caspase-3, a key downstream inducer of apoptosis, throughout the entirety of a CD8(+) T cell response. We utilized two infection models that differ in the intensity, onset and duration of antigen-presentation and inflammation. Expression of cleaved caspase-3 in antigen specific CD8(+) T cells was coupled to the timing and strength of antigen presentation in lymphoid organs. We also observed coordinated activation of additional canonical apoptotic markers, including phosphatidylserine exposure. Limiting dilution analysis directly showed that in the presence of IL7, very little cell death occurred in both caspase-3(hi) and caspase-3(low) CD8(+) T cells. The expression of active caspase-3 peaked before effector phenotype (CD62L(low)) CD8(+) T cells emerged, and was undetectable in effector-phenotype cells. In addition, OVA-specific CD8(+) cells remained active caspase-3(low) throughout the contraction phase.
conclusionsOur results specifically implicate antigen and not inflammation in driving activation of apoptotic mechanisms without cell death in proliferating CD8(+) T cells. Furthermore, the contraction of CD8(+) T cell response following expansion is likely not mediated by the key downstream apoptosis inducer, caspase-3.
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