Ontology highlight
ABSTRACT:
PROVIDER: PRJEB22015 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of peptide presentation by Human Leukocyte Antigen (HLA) class I of influenza B infected C1R cells expressing HLA-B*07:02, -B*08:01 or -B*35:01.
2024-03-04 | PXD045000 | Pride
Project description:The peptide identification sensitivity of the affinity purified immunopeptidome of a JY cell line (Epstein–Barr virus-immortalized B cell lymphoblastoid line, ECACC 94022533, IHW9287) for DDA and DIA experiments was assessed by a linear concentration series. JY cells are homozygous for all HLA-I loci (HLA-A*02:01, HLA-B*07:02, and HLA-C*07:02). The JY HLA-I ligandome was isolated through immunoaffinity purification, as described in Marcu, Bichmann and Kuchenbecker et al 2021.
2025-09-04 | PXD024809 | Pride
Project description:Here we report binding index of 305 human HLA class I molecules from 18,771 unique haplotypes of 28,104 individuals to the 821 peptides experimentally observed from spike protein receptor-binding domain (RBD) of 5 main SARS-CoV-2 strains hydrolysed by human proteasomes with constitutive and immuno catalytic phenotypes. Our data read that 4 point mutations in the C-terminal RBD region 496-505 of Omicron B1.1.529 strain results in a dramatic increase of proteasome-mediated release of two public HLA class I epitopes covering 82% and 27% of world population haplotypes. Global population analysis of HLA class I haplotypes specific to these peptides demonstrated decreased mortality of human populations bearing these haplotypes to COVID-19 after but not before December, 2021, when Omicron spread over the world and became dominant SARS-CoV-2 strain. Analysis of population frequency of HLA class I alleles revealed that HLA-B*07:02, -B*08:01, -B*15:01, -C*01:02, -C*06:02 and -C*07:02 potentially provides increased resistance of human population to Omicron. Concluding, we found direct experimental observation, which might be one of the key factors that forced the SARS-CoV-2 virus to cross back the red line of pandemic status.
2025-01-29 | PXD050265 | Pride
Project description:HLA-C expresion varies widely across the different HLA-C alleles. MicroRNA binding can partly explain the differences in HLA-C allele expression however other contributing factors still remain undetermined. Here we use two common HLA-C alleles, HLA-C*05:01 and HLA-C*07:02, to explore differences in expression levels. Using functional, structural and peptide repertoire comparisons we demonstrate that HLA-C expression levels are not only modulated at the RNA level but also at the protein level. This dataset contains RAW data and database search results for HLA-C*05:01 and HLA-C*07:02 from the 721.221 cell line.
2017-07-03 | PXD006455 | Pride
Project description:We identified epitopes derived from FOXM1 which were immunogenic on HLA-A*02:01, HLA-A*24:02, and HLA-A*23:01, endogenously-processed and presented, and resulted in T cell activation and cytotoxic T cell responses. Following the generation of TCR-T cells, sensitivity and specificity were confirmed by peptide dose-response and X-scan, respectively. Most importantly, adoptive transfer of TCR engineered T cells led to a significant reduction in tumor growth, as well as significantly prolonged survival in NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) tumor-bearing murine model. Our studies confirm the immunogenicity of FOXM1 and feasibility of targeting this antigen using TCR-engineering.
2026-03-11 | GSE319956 | GEO
Project description:Characterisation of peptide ligands of Major histocompatibility class (MHC) I isolated by immunoaffinity purification from the C1R (Class I reduced) B-lymphoblastoid cell line, transfected with the MHC class I allele HLA-A*01:01, or HLA-A*02:01, HLA-A*24:02. In addition, public mass spectrometry (MS) datasets of HLA-I and HLA-II immunopeptidome derived from patients’ samples, PBMC or cell lines, and shotgun proteomics from trypsin/elastase digestion were analysed.
2020-07-27 | PXD014754 | Pride
Project description:Identification of HLA-A*11:01 and A*02:01-restricted EBV Pep-tides using HLA Peptidomics
2024-06-14 | PXD051538 | Pride
Project description:DNA methyltransferase 3A (DNMT3A) and isocitrate dehydrogenase 1 & 2 (IDH1/2) are genes involved in epigenetic regulation, each mutated in 7-23% of acute myeloid leukemia (AML). Here, we investigated whether hotspot mutations in these genes encode neoantigens that can be targeted by immunotherapy. Five EBV-B cell lines expressing common HLA class I alleles were transduced with a minigene construct containing mutations that often occur in DNMT3A or IDH1/2. Peptides eluted from HLA class I alleles on these EBV-B cell lines were analyzed by tandem mass spec-trometry. We identified an HLA-A*01:01-binding DNMT3AR882H peptide and HLA-B*07:02-binding IDH2R140Q peptide, for which we searched for specific T cells in healthy individuals using pep-tide-HLA tetramers. Various T-cell clones were isolated showing specific reactivity against cell lines transduced with full-length DNMT3AR882H or IDH2R140Q genes, while cell lines transduced with wildtype genes were not recognized. One T-cell clone for DNMT3AR882H also reacted against patient AML cells with the mutation, while AML cells without the mutation were not recognized, thereby validating surface presentation of a DNMT3AR882H neoantigen that can potentially be targeted on HLA-A*01:01 positive AML by immunotherapy.
2024-06-23 | PXD050560 | Pride
Project description:Several HLA allelic variants have been associated with protection from, or susceptibility to infectious and autoimmune diseases. Here, we examined whether specific HLA alleles would be associated with different Mtb infection outcomes. We found that DQA1*03:01, DPB1*04:02, and DRB4*01:01 were signficantly more frequent in inividuals with active TB (susceptibility alleles). Furthermore, individuals who express any of the three susceptibility alleles were associated with lower magnitude of responses against Mtb antigens. We investigated the gene expression changes induced in PBMCs by Mtb lysate and a peptide pool (MTB300) in individuals with or without expression of the susceptibility alleles.
2023-03-29 | GSE207214 | GEO
Project description:T-cell based therapies have shown remarkable efficacy in multiple myeloma (MM), yet the disease remains largely incurable. Here, we investigated the constant domains of the immunoglobulin heavy chain (IgH) as novel targets for therapeutic T-cell receptors (TCRs), after confirming high and homogeneous IGH expression in >95% of MM patients. MM cells secrete excessive monoclonal immunoglobulins (M-proteins) that drive complications but are inaccessible to CAR T-cell or antibody targeting. Peptides from IgA and IgG constant regions were eluted from HLA-A*02:01, and reactive TCRs were isolated from healthy donors using allo-HLA-A*02:01 presentation to circumvent self-tolerance. T cells engineered with two TCRs specific for IgA or IgG passed a stringent multi-tier safety screen and selectively eliminated MM cells from 20 HLA-A*02:01+ patients secreting the relevant IgH in vitro. In vivo, IgA-TCR T cells eradicated IgA+HLA-A*02:01+ MM cells in xenograft models and reduced circulating IgA in humanized PBMC mice. These findings establish immunoglobulin constant domains as viable TCR targets in MM, potentially making ~40% of patients of European descent eligible for TCR T cell therapy, and extension to additional HLA alleles could further broaden eligibility. The approach may also be applicable to lymphoma and antibody-mediated autoimmune diseases.
2026-03-06 | PXD071196 | Pride