ArticleOncotarget2017
A cellular platform for the evaluation of immune checkpoint molecules.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
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.
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Who cites it
51 citing papers in PubMed, 75 citations in OpenAlex.
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- Distinctive features of the tumor and immune microenvironment in glioblastoma.NPJ precision oncology · 2026Article
- IL-18 metabolically reprograms CAR-expressing natural killer T cells and enhances their antitumor activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Scaffolding-dependent CASP1 constrains excessive cell-intrinsic inflammatory signaling in leukemia.Cell chemical biology · 2026Article
- Evaluation of Immune Checkpoint Inhibitors in a Jurkat-Based Transcriptional Reporter System: A Cell-Based Reporter Platform for Evaluation of Immune Checkpoint Inhibitors.Methods in molecular biology (Clifton, N.J.) · 2026Article
- CD160-Derived Peptide as a Bidirectional Inhibitor Toward Immune Checkpoints BTLA/HVEM and HVEM/LIGHT.Journal of medicinal chemistry · 2025Article
- Tracking NF-kB activity across steady-state neutrophil maturation.Cell death discovery · 2025Article
- Development of iPSC-derived T cells targeting EGFR neoantigens in non-small cell lung cancer.Molecular therapy. Methods & clinical development · 2025Article
- Platforms for studying cell-cell recognition by immune cells.Immunology and cell biology · 2025Review
- LAG-3-An incompletely understood target in cancer therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Mechanical force regulates ligand binding and function of PD-1.Nature communications · 2024Article
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- Dual role of the peptide-loading complex as proofreader and limiter of MHC-I presentation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The CD6 interactome orchestrates ligand-independent T cell inhibitory signaling.Cell communication and signaling : CCS · 2024Article
- Inhibitory CARs fail to protect from immediate T cell cytotoxicity.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Assessing the functional potential of conditioned media derived from amniotic epithelial stem cells engineered on 3D biomimetic scaffolds: An in vitro model for tendon regeneration.Materials today. Bio · 2024Article
- Article
- A high-throughput two-cell assay for interrogating inhibitory signaling pathways in T cells.Life science alliance · 2024Article
- Interrogating ligand-receptor interactions using highly sensitive cellular biosensors.Nature communications · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Blockade of the T cell coinhibitory molecules CTLA-4 and PD-1 has clinical utility to strengthen T cell responses. In addition to these immune checkpoints an ever-growing number of molecules has been implicated in generating coinhibitory signals in T cells. However, investigating coinhibitory molecules in primary human cells is complicated by the restricted expression and promiscuity of both coinhibitory receptors and their ligands. Here we have evaluated the potential of fluorescence-based transcriptional reporters based on the human Jurkat T cell line in conjunction with engineered T cell stimulator cell lines for investigating coinhibitory pathways. CTLA-4, PD-1, TIGIT, BTLA and 2B4 expressing reporter cells were generated and activated with T cell stimulator cells expressing cognate ligands of these molecules. All accessory molecules tested were functional in our reporter system. Engagement of CTLA-4, PD-1, BTLA and TIGIT by their ligands significantly inhibited T cell activation, whereas binding of 2B4 by CD48 resulted in enhanced responses. Mutational analysis revealed intracellular motifs that are responsible for BTLA mediated T cell inhibition and demonstrates potent reporter inhibition by CTLA-4 independent of cytoplasmic signaling motifs. Moreover, considerably higher IC50 values were measured for the CTLA-4 blocker Ipilimumab compared to the PD-1 antibody Nivolumab. Our findings show that coinhibitory pathways can be evaluated in Jurkat-based transcriptional reporters and yield novel insights on their function. Results obtained from this robust reductionist system can complement more time consuming and complex studies of such pathways in primary T cells.
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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.