ArticleNature communications2024
Cell softness renders cytotoxic T lymphocytes and T leukemic cells resistant to perforin-mediated killing.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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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.
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Who cites it
28 citing papers in PubMed, 27 citations in OpenAlex.
- Platycodon grandiflorus-Derived Nanovesicles Sensitize Gastric Cancer to T Cell Killing via Ferroptosis-Driven Membrane Mechanical Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Actin conformation dynamics precede force generation in cytotoxic T lymphocytes.Communications biology · 2026Article
- Differential perforin sensitivity drives lineage-dependent resistance to CAR T-cell killing in blood cancer cell lines.Blood advances · 2026Article
- Cofilin1-driven cytoskeletal remodeling modulates pan-cancer CD8Cell reports. Medicine · 2026Article
- Mechanical regulation of immunity in metastasis.Nature materials · 2026Article
- Mechanobiology of CAR-T cell therapy: regulatory mechanisms and strategies for enhanced antitumor immunity.Journal of translational medicine · 2026Review
- Identifying and reprogramming softness-driven cancer stem-like cells overcomes CAR-T cell resistance in solid tumours.Nature biomedical engineering · 2026Article
- Colorectal cancers with distinct metastatic potential trigger divergent early T cell responses.bioRxiv : the preprint server for biology · 2026Article
- Emerging role of microRNAs as modulators of the tumor immune microenvironment.Journal for immunotherapy of cancer · 2026Review
- Ionic regulation of cancer cell stiffness and metastatic colonization via the MRTFA-KCNMB1 axis.Developmental cell · 2026Article
- Transformative biomechanics and mechanobiology breakthroughs shaping the future of health and medicine.Innovation (Cambridge (Mass.)) · 2026Review
- Cytoskeletal prestress homeostasis is a biological principle that governs living cell structure and function.Mechanobiology in medicine · 2026Review
- Ionic Regulation of Mechanosurveillance and Metastasis via the MRTFA/KCNMB1 Axis.bioRxiv : the preprint server for biology · 2026Article
- A multidimensional workflow profiling of allogeneic virus-specific T cell therapies reveals potency-linked signatures.Nature communications · 2026Article
- TGFβ induces an atypical EMT to evade immune mechanosurveillance in lung adenocarcinoma dormant metastasis.Nature cancer · 2026Article
- Mechanomedicine: Present state and future promise.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanotransduction in Shaping Immunity: Pathways, Crosstalk, and Pathophysiological Relevance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Disrupting membranes, controlling cell fate: the role of pore-forming proteins in cell death and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- The multifaceted role of YAP in the tumor microenvironment and its therapeutic implications in cancer.Experimental & molecular medicine · 2025Review
- Mechanoregulation of lymphocyte cytotoxicity.Nature reviews. Immunology · 2025Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
Abstract
Mechanical force contributes to perforin pore formation at immune synapses, thus facilitating the cytotoxic T lymphocytes (CTL)-mediated killing of tumor cells in a unidirectional fashion. How such mechanical cues affect CTL evasion of perforin-mediated autolysis remains unclear. Here we show that activated CTLs use their softness to evade perforin-mediated autolysis, which, however, is shared by T leukemic cells to evade CTL killing. Downregulation of filamin A is identified to induce softness via ZAP70-mediated YAP Y357 phosphorylation and activation. Despite the requirements of YAP in both cell types for softness induction, CTLs are more resistant to YAP inhibitors than malignant T cells, potentially due to the higher expression of the drug-resistant transporter, MDR1, in CTLs. As a result, moderate inhibition of YAP stiffens malignant T cells but spares CTLs, thus allowing CTLs to cytolyze malignant cells without autolysis. Our findings thus hint a mechanical force-based immunotherapeutic strategy against T cell leukemia.
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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 Socratic graph.