B-cell linera epitope prediction
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB24387 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sanjuan2013 - Evolution of HIV T-cell epitope, control model
Control model in which the virus targets a nonimmune cell type C (e.g., hepatocytes, epithelial cells, etc.), instead of T H
cells.
This model is described in the article:
Immune activation promotes evolutionary conservation of T-cell epitopes in HIV-1.
Sanjuán R, Nebot MR, Peris JB, Alcamí J.
PLoS Biol. 2013 Apr;11(4):e1001523
Abstract:
The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (TH cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient level can promote either T-cell epitope conservation or escape. We predict greater conservation for epitopes contributing significantly to total immune activation levels (immunodominance), and when TH cell infection is concomitant to epitope recognition (trans-infection). We suggest that HIV-driven immune activation in the lymph nodes during the chronic stage of the disease may offer a favorable scenario for epitope conservation. Our results also support the view that some pathogens draw benefits from the immune response and suggest that vaccination strategies based on conserved TH epitopes may be counterproductive.
This model is hosted on BioModels Database
and identified
by: MODEL1302180002
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2005-01-01 | MODEL1302180002 | BioModels
Project description:Sanjuan2013 - Evolution of HIV T-cell epitope, immune activation model
Model of cellular immune response against HIV.
This model is described in the article:
Immune activation promotes evolutionary conservation of T-cell epitopes in HIV-1.
Sanjuán R, Nebot MR, Peris JB, Alcamí J.
PLoS Biol. 2013 Apr;11(4):e1001523
Abstract:
The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (TH cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient level can promote either T-cell epitope conservation or escape. We predict greater conservation for epitopes contributing significantly to total immune activation levels (immunodominance), and when TH cell infection is concomitant to epitope recognition (trans-infection). We suggest that HIV-driven immune activation in the lymph nodes during the chronic stage of the disease may offer a favorable scenario for epitope conservation. Our results also support the view that some pathogens draw benefits from the immune response and suggest that vaccination strategies based on conserved TH epitopes may be counterproductive.
Note from the author:
this version of the model is more general that the one described in the paper. This is because: (i) it can consider simultaneously Th-epitope escape mutants, CTL-epitope escape mutants and full T-cell (Th and CTL) escape mutants, by setting the mutation rate of Th and CTL escape mutants to zero. (ii) It allows for back mutations, which were ignored in all the simulations shown in the paper. (iii) It allows for a fitness cost of escape mutants, which was set to zero in the article. (iv) pAPCs can be infected and produce viruses (the rate of viral production for pAPCs was set to zero in the paper).
This model is hosted on BioModels Database
and identified
by: MODEL1302180001
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2005-01-01 | MODEL1302180001 | BioModels
Project description:The aim of the study was to determine the epitope targeted by four different HumAbs and the cross-reactivity to linear peptide epitopes of 5 different Neisserial adesin A (NadA) variants. the HumAbs were diluted at 1:200 and incubated on a custom PepStar Peptide Microarray platform printed with 348 different peptides.
2018-03-07 | GSE98881 | GEO
Project description:The aim of the study was to determine the epitope targeted by four different HumAbs and the cross-reactivity to linear peptide epitopes of 10 different Neisserial Heparin Binding Antigen (NHBA) variants. the HumAbs were diluted at 1:60 and incubated on a custom PepStar Peptide Microarray platform printed with 561 different peptides.
2018-03-07 | GSE98882 | GEO
Project description:The aim of the study was to determine the epitope targeted by 5 different HumAbs and the cross-reactivity to linear peptide epitopes of 12 different factor H binding protein (fHbp) variants. The HumAbs were diluted at 1:200 and incubated on a custom PepStar Peptide Microarray platform printed with 363 different peptides.
2018-03-07 | GSE98879 | GEO
Project description:Identifying epitopes that T cells respond to is critical to understanding T cell-mediated immunity. Traditional multimer and other single cell assays often require large blood volumes and/or expensive HLA-specific reagents and provide limited phenotypic and functional information. Here, we present the Rapid TCR:Epitope Ranker (RAPTER) assay, a single cell RNA sequencing (scRNA-SEQ) method that uses primary human T cells and antigen presenting cells (APCs) to assess functional T cell reactivity at single cell resolution. Using hash-tag oligonucleotide (HTO) coding and T cell activation-induced markers (AIM), RAPTER defines paired epitope specificity and TCR sequence and can include RNA- and protein-level T cell phenotype information. We demonstrate that RAPTER identified specific reactivities to viral and tumor antigens at sensitivities as low as 0.15% of total CD8+ T cells, and deconvoluted low-frequency circulating HPV16-specific T cell clones from a cervical cancer patient. The specificities of TCRs identified by RAPTER for MART1, EBV, and influenza epitopes were functionally confirmed in vitro. In summary, RAPTER identifies low-frequency T cell reactivities using primary cells from low blood volumes, and the resulting paired TCR: ligand information can directly enable immunogenic antigen selection for vaccine epitope inclusion, antigen-specific TCR tracking, and TCR cloning for further therapeutic development.
2023-08-25 | GSE231977 | GEO
Project description:The aim of the study was to determine the epitope targeted by 31E10/E7 mouse monoclonal antibody (mAb) and the cross-reactivity to linear peptide epitopes of 10 different Neisserial Heparin Binding Antigen (NHBA) variants. mAb 31E10/E7 was diluted at 1:200 and incubated on a custom PepStar Peptide Microarray platform printed with 560 different peptides in three independent experiments.
2016-05-27 | GSE81377 | GEO
Project description:Rapid TCR:Epitope Ranker (RAPTER): A primary human T cell reactivity screening assay pairing epitope and TCR at single cell resolution
| PRJNA970348 | ENA
Project description:Efficient control of tumor progression by CD4 T cell epitope-based prime-boost therapeutic vaccination
| PRJNA733193 | ENA
Project description:Clonal expansion is a hallmark of adaptive immunity, and appears to be driven by high antigen-specific receptor avidity as shown by research using murine in vivo models. In humans, however, the functionality of antigen-specific T cell clonotypes that are recruited into primary and recall immune responses remains surprisingly elusive. In this regard, the vaccination program during the SARS-CoV-2 pandemic represented a unique research opportunity by provision of highly standardized cohorts of healthy human individuals receiving immunizations against a previously unseen antigen. Here, we analyzed 30 HLA-typed individuals before, short-term and long-term after three mRNA vaccinations against SARS-CoV-2. We performed an in-depth characterization of the magnitude, phenotype, clonal composition and functionality of antigen-specific CD8 T cell responses by ELISPOT, flow cytometry and single-cell RNA sequencing, including CITE seq of 130 surface antigens and 16 T cell epitope specificities. 89 T cell receptors (TCRs) covering three complete epitope-specific repertoires were re-expressed by CRISPR/Cas9-mediated orthotopic TCR replacement and tested for their avidity. TCR repertoires underwent continuous tailoring, with high TCR avidity being linked to both clonal persistence and expansion. However, epitope-specific repertoires also maintained diversity by concomitant contraction and new emergence of functional T cell clones over time. These data on the phenotype and clonal selection within human antigen-specific T cell responses instruct our understanding of human T cell biology and may guide the development of enhanced or novel vaccines.
2024-10-31 | GSE261967 | GEO