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nature portfolio transfer plasmid plenti-cmv-egfp-puro privacy policy sars-cov-2 peptide/hla-a02 antigens hanging-drop vapour-diffusion method advertising 5% n-octyl β-d-thioglucopyranoside pre-emptively predict cross-reactivities uk/pride/archive/projects/pxd027182 libraries prepared web portal human t-activator cd3/cd28 social media elisa kits exon-level expression timothy mage-a3 peptide presented h3k27ac super-enhancer elements biochemical large-scale identification childhood cancer research author information authors eliminate cross-reactive cars cross-reactive show killing h3k27ac super-enhancer mark produce replication-deficient lentivirus monitored bi-weekly measurements contract de-ac02-05ch11231 h3k27ac super-enhancer element high-risk mycn-amplified neuroblastoma insulin peptide cross-reactivity predicted cross-reactivity based moreno di marco 800 iu ml−1 gm-csf 600 iu ml−1 gm-csf tumour-specific membrane proteins5 normal-tissue ligandomic dataset single-antigen-specific population nature 500 nature 555 nature 571 nature 399 nature 599 nature potential cross-reactive peptides half-maximal inhibitory concentration peptide-centric scfv binders comprehensive python-based system steady-state binding assay m1 antigen-specific hybridoma graft-versus-host disease improved inter-species database

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         headline:RETRACTED ARTICLE: Cross-HLA targeting of intracellular oncoproteins with peptide-centric CARs
         description:The majority of oncogenic drivers are intracellular proteins, thus constraining their immunotherapeutic targeting to mutated peptides (neoantigens) presented by individual human leukocyte antigen (HLA) allotypes1. However, most cancers have a modest mutational burden that is insufficient to generate responses using neoantigen-based therapies2,3. Neuroblastoma is a paediatric cancer that harbours few mutations and is instead driven by epigenetically deregulated transcriptional networks4. Here we show that the neuroblastoma immunopeptidome is enriched with peptides derived from proteins that are essential for tumourigenesis and focus on targeting the unmutated peptide QYNPIRTTF, discovered on HLA-A*24:02, which is derived from the neuroblastoma dependency gene and master transcriptional regulator PHOX2B. To target QYNPIRTTF, we developed peptide-centric chimeric antigen receptors (CARs) using a counter-panning strategy with predicted potentially cross-reactive peptides. We further hypothesized that peptide-centric CARs could recognize peptides on additional HLA allotypes when presented in a similar manner. Informed by computational modelling, we showed that PHOX2B peptide-centric CARs also recognize QYNPIRTTF presented by HLA-A*23:01 and the highly divergent HLA-B*14:02. Finally, we demonstrated potent and specific killing of neuroblastoma cells expressing these HLAs in vitro and complete tumour regression in mice. These data suggest that peptide-centric CARs have the potential to vastly expand the pool of immunotherapeutic targets to include non-immunogenic intracellular oncoproteins and widen the population of patients who would benefit from such therapy by breaking conventional HLA restriction. Targeting peptides from unmutated cancer drivers that are expressed in tumours but not in normal tissues using peptide-centric chimeric antigen receptors shows potential as treatment for cancer.
         datePublished:2021-11-03T00:00:00Z
         dateModified:2023-11-08T00:00:00Z
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      headline:RETRACTED ARTICLE: Cross-HLA targeting of intracellular oncoproteins with peptide-centric CARs
      description:The majority of oncogenic drivers are intracellular proteins, thus constraining their immunotherapeutic targeting to mutated peptides (neoantigens) presented by individual human leukocyte antigen (HLA) allotypes1. However, most cancers have a modest mutational burden that is insufficient to generate responses using neoantigen-based therapies2,3. Neuroblastoma is a paediatric cancer that harbours few mutations and is instead driven by epigenetically deregulated transcriptional networks4. Here we show that the neuroblastoma immunopeptidome is enriched with peptides derived from proteins that are essential for tumourigenesis and focus on targeting the unmutated peptide QYNPIRTTF, discovered on HLA-A*24:02, which is derived from the neuroblastoma dependency gene and master transcriptional regulator PHOX2B. To target QYNPIRTTF, we developed peptide-centric chimeric antigen receptors (CARs) using a counter-panning strategy with predicted potentially cross-reactive peptides. We further hypothesized that peptide-centric CARs could recognize peptides on additional HLA allotypes when presented in a similar manner. Informed by computational modelling, we showed that PHOX2B peptide-centric CARs also recognize QYNPIRTTF presented by HLA-A*23:01 and the highly divergent HLA-B*14:02. Finally, we demonstrated potent and specific killing of neuroblastoma cells expressing these HLAs in vitro and complete tumour regression in mice. These data suggest that peptide-centric CARs have the potential to vastly expand the pool of immunotherapeutic targets to include non-immunogenic intracellular oncoproteins and widen the population of patients who would benefit from such therapy by breaking conventional HLA restriction. Targeting peptides from unmutated cancer drivers that are expressed in tumours but not in normal tissues using peptide-centric chimeric antigen receptors shows potential as treatment for cancer.
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         MHC class I
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