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| 001 | 298413 | ||
| 005 | 20251002115233.0 | ||
| 024 | 7 | _ | |a 10.1038/s41467-025-56547-w |2 doi |
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| 024 | 7 | _ | |a pmc:PMC11787355 |2 pmc |
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| 037 | _ | _ | |a DKFZ-2025-00269 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 500 |
| 100 | 1 | _ | |a Chih, Yu-Chan |0 P:(DE-He78)bc4a5e69aaad6fee8ca94e2f1d60b443 |b 0 |e First author |u dkfz |
| 245 | _ | _ | |a Vaccine-induced T cell receptor T cell therapy targeting a glioblastoma stemness antigen. |
| 260 | _ | _ | |a [London] |c 2025 |b Springer Nature |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1740748910_28237 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a #EA:D170#LA:D170# / DKFZ-ZMBH-Alliance / HI-TRON |
| 520 | _ | _ | |a T cell receptor-engineered T cells (TCR-T) could be advantageous in glioblastoma by allowing safe and ubiquitous targeting of the glioblastoma-derived peptidome. Protein tyrosine phosphatase receptor type Z1 (PTPRZ1), is a clinically targetable glioblastoma antigen associated with glioblastoma cell stemness. Here, we identify a therapeutic HLA-A*02-restricted PTPRZ1-reactive TCR retrieved from a vaccinated glioblastoma patient. Single-cell sequencing of primary brain tumors shows PTPRZ1 overexpression in malignant cells, especially in glioblastoma stem cells (GSCs) and astrocyte-like cells. The validated vaccine-induced TCR recognizes the endogenously processed antigen without off-target cross-reactivity. PTPRZ1-specific TCR-T (PTPRZ1-TCR-T) kill target cells antigen-specifically, and in murine experimental brain tumors, their combined intravenous and intracerebroventricular administration is efficacious. PTPRZ1-TCR-T maintain stem cell memory phenotype in vitro and in vivo and lyse all examined HLA-A*02+ primary glioblastoma cell lines with a preference for GSCs and astrocyte-like cells. In summary, we demonstrate the proof of principle to employ TCR-T to treat glioblastoma. |
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| 650 | _ | 7 | |a Receptors, Antigen, T-Cell |2 NLM Chemicals |
| 650 | _ | 7 | |a Cancer Vaccines |2 NLM Chemicals |
| 650 | _ | 7 | |a PTPRZ1 protein, human |0 EC 3.1.3.48 |2 NLM Chemicals |
| 650 | _ | 7 | |a HLA-A2 Antigen |2 NLM Chemicals |
| 650 | _ | 7 | |a Receptor-Like Protein Tyrosine Phosphatases, Class 5 |0 EC 3.1.3.48 |2 NLM Chemicals |
| 650 | _ | 7 | |a HLA-A*02 antigen |2 NLM Chemicals |
| 650 | _ | 7 | |a Antigens, Neoplasm |2 NLM Chemicals |
| 650 | _ | 2 | |a Glioblastoma: therapy |2 MeSH |
| 650 | _ | 2 | |a Glioblastoma: immunology |2 MeSH |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Animals |2 MeSH |
| 650 | _ | 2 | |a Receptors, Antigen, T-Cell: immunology |2 MeSH |
| 650 | _ | 2 | |a Receptors, Antigen, T-Cell: metabolism |2 MeSH |
| 650 | _ | 2 | |a Brain Neoplasms: immunology |2 MeSH |
| 650 | _ | 2 | |a Brain Neoplasms: therapy |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Neoplastic Stem Cells: immunology |2 MeSH |
| 650 | _ | 2 | |a Neoplastic Stem Cells: metabolism |2 MeSH |
| 650 | _ | 2 | |a Cell Line, Tumor |2 MeSH |
| 650 | _ | 2 | |a Cancer Vaccines: immunology |2 MeSH |
| 650 | _ | 2 | |a HLA-A2 Antigen: immunology |2 MeSH |
| 650 | _ | 2 | |a HLA-A2 Antigen: metabolism |2 MeSH |
| 650 | _ | 2 | |a HLA-A2 Antigen: genetics |2 MeSH |
| 650 | _ | 2 | |a T-Lymphocytes: immunology |2 MeSH |
| 650 | _ | 2 | |a T-Lymphocytes: metabolism |2 MeSH |
| 650 | _ | 2 | |a Immunotherapy, Adoptive: methods |2 MeSH |
| 650 | _ | 2 | |a Receptor-Like Protein Tyrosine Phosphatases, Class 5: metabolism |2 MeSH |
| 650 | _ | 2 | |a Receptor-Like Protein Tyrosine Phosphatases, Class 5: genetics |2 MeSH |
| 650 | _ | 2 | |a Antigens, Neoplasm: immunology |2 MeSH |
| 650 | _ | 2 | |a Antigens, Neoplasm: metabolism |2 MeSH |
| 650 | _ | 2 | |a Female |2 MeSH |
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| 773 | _ | _ | |a 10.1038/s41467-025-56547-w |g Vol. 16, no. 1, p. 1262 |0 PERI:(DE-600)2553671-0 |n 1 |p 1262 |t Nature Communications |v 16 |y 2025 |x 2041-1723 |
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