ArticleNature communications2025
CD99-mediated immunological synapse formation potentiates CAR-T cell function.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed.
- Enhancing persistence while managing cytokine release syndrome to embrace next-generation CAR-T cell therapy.Journal of translational medicine · 2026Review
- ESM1 drives cancer angiogenesis and bevacizumab resistance via trioleate synthesis.Neoplasia (New York, N.Y.) · 2026Article
- Article
- Interaction of CD99 and its ligands regulates immunoregulatory pathways in NK cells.Frontiers in immunology · 2026Article
- CD99-targeted immunomagnetic negative selection: A novel strategy for high-purity pancreatic islet isolation in murine models.PloS one · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Despite the efficacy of chimeric antigen receptor (CAR)-T cells in selected hematological malignancies, further improvement on CAR-T designs is still desirable. We hypothesize that modifying the CAR structure to enhance immunological synapse (IS) stabilization and CAR target-binding may be a feasible strategy. Here we show that the membrane protein, CD99, is critical for IS formation in T cells by mediating actin-microtubule interaction. CD99 deficiency abolishes IS formation and prevents effective in vivo T cell immunity. Mechanistically, CD99 interacts with microtubules and actins through the transmembrane and cytoplasmic domains, respectively, with which myosin and IQGAP1 interact. As such, incorporating the transmembrane and juxtamembrane domains of CD99 into the CAR structure enhances IS formation and improves the therapeutic efficacy of human CAR-T cells against lymphoma in immune-deficient mice. Our data thus suggest that CD99-mediated IS stabilization may help improve CAR design and efficacy.
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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.