ArticleNature communications2022
Differential trafficking of ligands trogocytosed via CD28 versus CTLA4 promotes collective cellular control of co-stimulation.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Programmable macromolecule delivery via engineered trogocytosis.Nature cell biology · 2026Article
- Next-Generation Immune Checkpoints and Tumor Microenvironment Modulation in Cancer Immunotherapy.Journal of immunology research · 2026Review
- Treatment with saturating dose of conventional anti-CD28 monoclonal antibody well tolerated in pig acute myocardial infarction model.Frontiers in immunology · 2026Article
- Chromosome Missegregation Triggers Tumor Cell Pyroptosis and Enhances Anti-Tumor Immunotherapy in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MHC class I-dressing is mediated via phosphatidylserine recognition and is enhanced by polyI:C.iScience · 2024Article
- Trogocytosis of CAR molecule regulates CAR-T cell dysfunction and tumor antigen escape.Signal transduction and targeted therapy · 2023Article
- Review
- Deletion of the inhibitory co-receptor CTLA-4 enhances and invigorates chimeric antigen receptor T cells.Immunity · 2023Article
- Immune checkpoint therapy for solid tumours: clinical dilemmas and future trends.Signal transduction and targeted therapy · 2023Review
- CTLA4 prohibits T cells from cross-dressing.The Journal of experimental medicine · 2023Article
- CTLA4 depletes T cell endogenous and trogocytosed B7 ligands via cis-endocytosis.The Journal of experimental medicine · 2023Article
- The Concordant Disruption of B7/CD28 Immune Regulators Predicts the Prognosis of Oral Carcinomas.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intercellular communication is crucial for collective regulation of cellular behaviors. While clustering T cells have been shown to mutually control the production of key communication signals, it is unclear whether they also jointly regulate their availability and degradation. Here we use newly developed reporter systems, bioinformatic analyses, protein structure modeling and genetic perturbations to assess this. We find that T cells utilize trogocytosis by competing antagonistic receptors to differentially control the abundance of immunoregulatory ligands. Specifically, ligands trogocytosed via CD28 are shuttled to the T cell surface, enabling them to co-stimulate neighboring T cells. In contrast, CTLA4-mediated trogocytosis targets ligands for degradation. Mechanistically, this fate separation is controlled by different acid-sensitivities of receptor-ligand interactions and by the receptor intracellular domains. The ability of CD28 and CTLA4 to confer different fates to trogocytosed ligands reveals an additional layer of collective regulation of cellular behaviors and promotes the robustness of population dynamics.
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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.