ArticlePloS one2013
Regulation of A1 by OX40 contributes to CD8(+) T cell survival and anti-tumor activity.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Harnessing cancer immunotherapy during the unexploited immediate perioperative period.Nature reviews. Clinical oncology · 2020Review
- Review
- Fates of CD8+ T cells in Tumor Microenvironment.Computational and structural biotechnology journal · 2019Review
- Dying to protect: cell death and the control of T-cell homeostasis.Immunological reviews · 2017Review
- The BCL-2 pro-survival protein A1 is dispensable for T cell homeostasis on viral infection.Cell death and differentiation · 2017Article
- C-Myc regulation by costimulatory signals modulates the generation of CD8+ memory T cells during viral infection.Open biology · 2016Article
- Melanoma Immunotherapy in Mice Using Genetically Engineered Pluripotent Stem Cells.Cell transplantation · 2016Article
- Advances in immunotherapy for treatment of lung cancer.Cancer biology & medicine · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
The TNFR family member OX40 (CD134) is critical for optimal clonal expansion and survival of T cells. However, the intracellular targets of OX40 in CD8 T cells are not fully understood. Here we show that A1, a Bcl-2 family protein, is regulated by OX40 in effector CD8 T cells. In contrast to wild-type T cells, OX40-deficient CD8 T cells failed to maintain A1 expression driven by antigen. Conversely, enforced OX40 stimulation promoted A1 expression. In both situations, the expression of A1 directly correlated with CD8 T cell survival. In addition, exogenous expression of A1 in OX40-deficient CD8 T cells reversed their survival defect in vitro and in vivo. Moreover, forced expression of A1 in CD8 T cells from OX40-deficient mice restored the ability of these T cells to suppress tumor growth in a murine model. These results indicate that OX40 signals regulate CD8 T cell survival at least in part through maintaining expression of the anti-apoptotic molecule A1, and provide new insight into the mechanism by which OX40 may impact anti-tumor immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.