ArticleOncotarget2017
Tumor regression is mediated via the induction of HER263-71- specific CD8+ CTL activity in a 4T1.2/HER2 tumor model: no involvement of CD80 in tumor control.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- A Membrane Fluidization Strategy Significantly Boosts Photodynamic Therapy and Antitumor Immunity of Porphyrin-Lipid Nanoparticles.ACS nano medicine · 2026Article
- Functional Suitability Evaluation of Radioimmunoconjugates of Nanobodies against PD-L1 and HER2/neu for Tumor Theranostics.Sovremennye tekhnologii v meditsine · 2026Article
- Synergistic Anticancer Activity of Fucoidan fromMarine drugs · 2025Article
- Chimeric antigen receptor macrophages (CAR-M) sensitize HER2+ solid tumors to PD1 blockade in pre-clinical models.Nature communications · 2025Article
- Cell Model for Testing Pharmaceuticals Targeting Human PD-L1.Sovremennye tekhnologii v meditsine · 2024Article
- Syngeneic mouse model of human HER2+ metastatic breast cancer for the evaluation of trastuzumab emtansine combined with oncolytic rhabdovirus.Frontiers in immunology · 2023Article
- B16 melanoma control by anti-PD-L1 requires CD8+ T cells and NK cells: application of anti-PD-L1 Abs and Trp2 peptide vaccines.Human vaccines & immunotherapeutics · 2021Article
- Regulation of the translation activity of antigen-specific mRNA is responsible for antigen loss and tumor immune escape in a HER2-expressing tumor model.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the CT26/HER2 and 4T1.2/HER2 tumor models, CT26/HER2 cells form tumors that continue to grow, whereas 4T1.2/HER2 cells form tumors that eventually regress. Here, we investigated the differences in the behaviors of these two cell lines. When immune cells from 4T1.2/HER2 tumor-bearing animals were stimulated with HER2 class I peptides, they displayed a 2-fold increase in IFN-γ levels, in response to the peptides, HER263-71 and HER2342-350. In contrast, extremely high levels of antigen-non-specific IFN-γ production were observed with immune cells and sera from CT26/HER2 tumor-bearing mice. However, IFN-γ had no effect on tumor progression in the CT26/HER2 model, as determined by an IFN-γ knockout assay. 4T1.2/HER2 tumor-bearing mice displayed CTL activity in response to HER263-71 but not to HER2342-350, whereas no such induction was observed in CT26/HER2 tumor-bearing mice. When 4T1.2/HER2 cell-challenged mice were depleted of CD8+ T cells, they lost their tumor-regressing activity, suggesting an antitumor role of HER263-71-specific CD8+ CTLs in the control of this tumor type. CT26/HER2 cells also expressed CD80. However, CD80-transfected 4T1.2/HER2 and CD80-non-expressing CT26/HER2 cells failed to alter their tumorigenicity, suggesting no role of CD80 in tumor control. Despite increased levels of myeloid-derived suppressor cells in the tumor, they were not associated with tumor progression in the CT26/HER2 model, as determined by a cell depletion assay. Overall, these data show that, contrary to CT26/HER2 tumors, 4T1.2/HER2 tumors regress via the induction of HER263-71-specific CD8+ CTLs and that CD80 is not associated with the regression of these tumors.
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