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: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: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:The Human leukocyte antigen (HLA) -region, especially HLA class I and II genes, plays a major role in the predisposition to autoimmune disorders. Particularly three HLA haplotypes, DRB1*03-DQA1*05-DQB1*02 (DR3-DQ2), DRB1*04:01-DQA1*03-DQB1*03:02 (DR4-DQ8) and DRB1*15-DQA1*01-DQB1*06:02 (DR2-DQ6), have an important role in many autoimmune diseases: for example, in type 1 diabetes (T1D) the DR2-DQ6 is associated with a strongly decreased T1D risk and the DR3-DQ2 and DR4-DQ8 are associated with a moderately increased T1D risk. To clarify the mechanisms behind this association, we examined genome-wide DNA methylation in CD4+ T cells and CD19+ B cells of healthy subjects homozygous either for DR3-DQ2 (n = 19), DR4-DQ8 (n = 17) or DR2-DQ6 (n = 14), and compared methylation between the genotypes. For the study, CD4+ T cells and CD19+ B cells were isolated consecutively from PBMC samples using magnetic bead separation. DNA was extracted from the cell lysates with AllPrep DNA/RNA/miRNA Universal Kit (Qiagen, Germany). Then the individual DNA samples were pooled into 11 pooled samples with 4–5 samples per pooled sample. The original 50 samples were designated pools based on age and sex to ensure that the age and sex distributions would be as similar as possible between the pooled samples. The mean age (±SD) in the three HLA-groups (DR2-DQ6, DR3-DQ2 and DR4-DQ8) were 15.0 (±8.3), 11.1 (±5.6) and 11.8 (±7.9) and their male to female ratios were 8/6, 9/10 and 11/6. Similar pooled samples were created for both the CD4+ T cell and the CD19+ B cell samples. Then DNA methylation was examined in the pooled CD4+ T cell and CD19+ B cell samples using Illumina Infinium HumanMethylation EPIC beadchip.
2024-06-20 | E-MTAB-13654 | biostudies-arrayexpress
Project description:Whether the presentation levels of the major histocompatibility complex (MHC, called the human leukocytes antigens, HLA, in humans) is limited by the availability of peptide ligands for loading or by the supply of empty MHC molecules, is a yet unresolved issue. This study aims to tackle this dilemma using large-scale immunopeptidome analyses. First, cultured cells (MCF-7) were treated with interferons, which dramatically increased presentation levels of their HLA-B molecules, much more than HLA-A and HLA-C. The differential increase in the HLA-B molecules with their bound peptides, was driven by elevated HLA synthesis levels and not by supply of peptides, since all three HLA allotypes draw peptides from the same peptide pool, which should have been affected similarly by the interferons treatment. In addition, artificial competition for peptides was created by recombinant high levels expression of soluble HLA-A*02:01 molecules, in the same MCF-7 cells and on top of their endogenous membranal HLA-A*02:01. This high level expression of the soluble HLA did not affect the endogenous membranal HLA-A*02:01 peptidomes or its cell surface presentation levels. We therefore concluded that a surplus supply of peptides is available for loading and that presentation levels are more likely limited by the supply of HLA molecules.
2018-05-10 | PXD007596 | Pride
Project description:Somatic mutations in cancer are a potential source of cancer specific neoantigens. Acute myeloid leukemia (AML) has common recurrent mutations shared between patients in addition to private mutations specific to individuals. We hypothesized that neoantigens derived from recurrent shared mutations would be attractive targets for future immunotherapy and sought to study the Class I and II HLA ligandomes of thirteen primary AML tumor samples and two AML cell lines (OCI-AML3 and MV4-11) using mass spectrometry. We identified two endogenous, mutation-bearing HLA Class I ligands from NPM1, which are predicted to bind the common HLA haplotypes, HLA-A*03:01 and HLA-A*02:01 respectively. We further derived CD8+ T cells from healthy donor peripheral blood samples which bound mutant-peptide loaded A*03:01 and A*02:01 tetramers, suggesting a new source of NPM1 mutation-specific T cell receptors (TCRs) for future evaluation. Since NPM1 is mutated in approximately one-third of patients with AML, the finding of endogenous NPM1 neoantigens supports future studies evaluating immunotherapeutic approaches against this target, for this subset of patients with AML.
2019-07-17 | PXD012083 | Pride