ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Cleavage of anti-apoptotic Bcl-2 family members after TCR stimulation contributes to the decision between T cell activation and apoptosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Combining MCL-1 inhibition and CD37-directed chimeric antigen receptor T cells as an effective strategy to target T-cell lymphoma.Leukemia · 2025Article
- Leucine zipper-based immunomagnetic purification of CAR T cells displaying multiple receptors.Nature biomedical engineering · 2024Article
- TIM-3 drives temporal differences in restimulation-induced cell death sensitivity in effector CD8Cell death & disease · 2021Article
- JNK1 and ERK1/2 modulate lymphocyte homeostasis via BIM and DRP1 upon AICD induction.Cell death and differentiation · 2020Article
- Control of Immunoregulatory Molecules by miRNAs in T Cell Activation.Frontiers in immunology · 2018Review
- The Antitumor Effects of Vaccine-Activated CD8Cancer immunology research · 2017Article
- The Ebola Interferon Inhibiting Domains Attenuate and Dysregulate Cell-Mediated Immune Responses.PLoS pathogens · 2016Article
- Macroautophagy inhibition maintains fragmented mitochondria to foster T cell receptor-dependent apoptosis.The EMBO journal · 2016Article
- Article
- Protective effect of bone marrow mesenchymal stem cells on PC12 cells apoptosis mediated by TAG1.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Engagement of the TCR induces activation-induced cell death (AICD) of T cells that have been previously stimulated. However, a portion of these T cells can survive and undergo further activation. The molecular mechanism that decides whether a T cell will live or die after TCR re-engagement is unclear. We found that cross-linking of TCR in preactivated primary mouse T cells led to the cleavage of anti-apoptotic Bcl-2 and Bcl-xL in dying cells. Cleavage-resistant Bcl-2 and Bcl-xL were more efficient than their wild-type counterparts in the inhibition of apoptosis in primary mouse T cells and in the H9 T cell line after TCR cross-linking. In contrast, the surviving T cells after TCR re-engagement displayed upregulation of Bcl-xL, and knockdown of Bcl-xL promoted AICD. This indicates that caspase-mediated cleavage of anti-apoptotic Bcl-2 or Bcl-xL facilitates AICD in T cells, whereas upregulation of Bcl-xL promotes T cell survival and allows further T cell activation. Our data suggest that cleavage of anti-apoptotic Bcl-2 and Bcl-xL contributes to the decision between T cell activation and apoptosis after TCR re-engagement.
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Registered trials
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