Ontology highlight
ABSTRACT:
PROVIDER: PRJNA673228 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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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.
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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: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: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
Project description:Immunopeptidomes are the peptide repertoires bound by the molecules encoded by the major histocompatibility complex (MHC) (human leukocyte antigen (HLA) in humans). These HLA-peptide complexes are presented on the cell surface for immune T cell recognition. Immunopeptidomics utilizes tandem mass spectrometry (MS/MS) to identify and quantify peptides bound to HLA molecules. The dataset deposited here contains the DDA runs used to generate the spectral libraries of the HLA-bound peptides purified and isolated from C1R-B*57:01 and C1R-A*02:01 cell lines.
2023-02-13 | PXD034429 | Pride
Project description:This dataset contains further evidence that the HLA-A*02:01+ KRAS G12V+ spliced neoepitope we previously identified (Mishto et al., Front. Immunol. 2019) is produced by proteasomes in various experimental conditions
2022-09-05 | PXD024528 | Pride
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