ArticleThe Journal of physiology2003
The actin cytoskeleton and cytotoxic T lymphocytes: evidence for multiple roles that could affect granule exocytosis-dependent target cell killing.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Phosphatases in tumor cell immune escape: a perspective based on the camouflage, coercion, cytoprotection.Frontiers in cell and developmental biology · 2026Review
- Protein lipidation in the tumor microenvironment: enzymology, signaling pathways, and therapeutics.Molecular cancer · 2025Review
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- STIM Proteins and Regulation of SOCE in ER-PM Junctions.Biomolecules · 2022Review
- Measuring expression heterogeneity of single-cell cytoskeletal protein complexes.Nature communications · 2021Article
- Targeting the Microtubule-Network Rescues CTL Killing Efficiency in Dense 3D Matrices.Frontiers in immunology · 2021Article
- Migrastatics-Anti-metastatic and Anti-invasion Drugs: Promises and Challenges.Trends in cancer · 2017Review
- Article
- The cytoskeletal adaptor protein IQGAP1 regulates TCR-mediated signaling and filamentous actin dynamics.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Non-catalytic functions of Pyk2 and Fyn regulate late stage adhesion in human T cells.PloS one · 2012Article
- Natural killer cell lytic granule secretion occurs through a pervasive actin network at the immune synapse.PLoS biology · 2011Article
- Regulation of retinoschisin secretion in Weri-Rb1 cells by the F-actin and microtubule cytoskeleton.PloS one · 2011Article
- Distinct role of rab27a in granule movement at the plasma membrane and in the cytosol of NK cells.PloS one · 2010Article
- The human fungal pathogen Cryptococcus neoformans escapes macrophages by a phagosome emptying mechanism that is inhibited by Arp2/3 complex-mediated actin polymerisation.PLoS pathogens · 2010Article
- Calcineurin-dependent lytic granule exocytosis in NK-92 natural killer cells.Cellular immunology · 2009Article
- ERK activation is only one role of PKC in TCR-independent cytotoxic T cell granule exocytosis.Biochemical and biophysical research communications · 2008Article
- Contributions to our understanding of T cell physiology through unveiling the T cell proteome.Clinical and experimental immunology · 2007Review
- Tyrosine kinase activity and remodelling of the actin cytoskeleton are co-temporally required for degranulation by cytotoxic T lymphocytes.Immunology · 2005Article
- Exocytic responses of single leukaemic human cytotoxic T lymphocytes stimulated by agents that bypass the T cell receptor.The Journal of physiology · 2005Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
One important mechanism cytotoxic T lymphocytes (CTLs) use to kill virus-infected, transplanted or tumour targets is exocytosis of granules that contain cytotoxic agents such as perforin and granzymes. Granule exocytosis-dependent target cell killing is a complex process, involving initial T-cell receptor (TCR)-dependent signalling that includes Ca2+ influx and activation of protein kinase C, shape changes that serve to bind the CTL to the target and, finally, exocytosis of lytic granules at the site of contact with the target cell. Although there is reason to propose that multiple steps in the lytic process could involve the actin cytoskeleton of CTLs, few studies have examined this issue, and those that have do not allow the specific step(s) involved to be determined. We have used the potent membrane-permeant actin cytoskeleton-modifying drugs jasplakinolide and latrunculin A to investigate the actin dependence of defined processes that are expected to be important for granule exocytosis-dependent killing. Our results, obtained using TALL-104 human leukaemic CTLs as a model system, are consistent with the idea that a functional actin cytoskeleton is required for TCR/CD3-dependent signalling, for activation of store-dependent Ca2+ influx and for CTL shape changes. When cells were stimulated with solid-phase anti-CD3 antibodies, treatment with either jasplakinolide or latrunculin A abolished granule exocytosis. However, when cells were stimulated in a manner that bypasses TCR/CD3-dependent signalling, granule exocytosis was not significantly altered, suggesting that the actin cytoskeleton does not function as a barrier to exocytosis.
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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.