ArticleThe Journal of experimental medicine2026
Chimeric MHC class I- and II-restricted non-self epitopes broaden antitumor T cell reactions.
Article in The Journal of experimental medicine, 2026. 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.
- Autocrine Control of CD276 by SPARC in Liver Cancer and Its Contribution to Immune Escape and Resistance to Immunotherapy: Elucidating How SPARC Shapes the Tumor Microenvironment and Undermines the Response to Immune Checkpoint Inhibition.Journal of biochemical and molecular toxicology · 2026Article
- The Central Role of HLA Class II-Restricted Helper Neoantigen Vaccines in Cancer Immunotherapy.Cancers · 2026Review
- Bright side of the dark genome: antigens for next-gen cancer vaccines.Journal for immunotherapy of cancer · 2026Review
- High resolution immunoinformatic profiling of Zonula occludens toxin reveals a conserved multiepitope vaccine candidate inFrontiers in immunology · 2026Article
- Adipose-Derived Mesenchymal Stem Cells Reduce miR-214-5p to Promote Ovarian Cancer Progression via the β-Catenin Pathway by Targeting PAX8.Stem cells international · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The mechanism by which one non-self antigen augments T cell immune responses to another remains unclear. We found that these expanded immune responses could derive from chimeric non-self peptides. These peptides, which we termed complete T cell antigens (CTAs), must be expressed intracellularly as single-chain chimeras containing both MHC class I- and II-restricted epitopes. CTAs, even unrelated to tumor antigens, when administered as live cell adjuvants or in cDNA-transfected muscle, increased T cell reactivity against tumor neoantigens. Mechanistically, CTA treatment altered dendritic cell phenotype in a CD4+ T cell-dependent manner, suppressing CD8+ T cell exhaustion and generating self-renewing CD8+ T cells in tumors. Cancers predicted to have long non-self peptides resulting from frameshift mutations, which frequently contain CTAs, were associated with a better prognosis or benefit from PD-1 blockade therapy in mouse models and cancer patients. These findings indicate that a subset of cancer cells expressing CTAs is sufficient to evoke overall antitumor immunity by broadening T cell responses to other neoantigens.
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Registered trials
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