B-cell linera epitope prediction
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ABSTRACT:
PROVIDER: PRJEB24387 | ENA |
REPOSITORIES: ENA
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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:The vascular endothelial growth factor A (VEGF) is involved in various physiological processes such as angiogenesis or wound healing but is also crucial in pathological events such as tumor growth. Thus, clinical anti-VEGF treatments have been developed which could already prove to have enormous beneficial effects for cancer patients. In this article we describe the first VEGF-derived CD8+ T-cell epitope. The natural HLA ligand SRFGGAVVR was identified by differential mass spectrometry in two primary renal cell carcinomas (RCC) and was significantly over-presented on both tumor tissues. SRFGGAVVR is derived from a cryptic translated region of VEGF presumably by initiation of translation at the non-classical start codon CUG499. SRFGGAVVR specific T-cells were generated in vitro using peptide loaded dendritic cells or artificial antigen presenting cells. They were identified by HLA tetramer analysis after in vitro stimulation. SRFGGAVVR specific CD8+ T-cells were fully functional T-effector cells, which were able to secrete IFN-gamma upon stimulation and killed tumor cells in vitro. Additionally, we have quantitatively analyzed VEGF mRNA and protein levels in RCC tumor and normal tissue samples by gene chip analysis, qRT-PCR, in situ hybridization, and bead based immuno assay. In the future, T-cells directed against VEGF as a tumor associated antigen may represent a possible way of combining peptide-based anti-VEGF immunotherapy with already existent anti-VEGF cancer therapies. Experiment Overall Design: Two clear cell renal cell carcinomas including autologous normal tissue were analyzed.
2008-06-15 | E-GEOD-8050 | biostudies-arrayexpress
Project description:Dengue and Zika are two mosquito-borne diseases of great concern, affecting mainly the tropical and subtropical regions worldwide. The arrival of Zika virus (ZIKV) in dengue virus (DENV) endemic areas imposed challenges for differential diagnosis and the development of candidate vaccines. The use of peptides has shown great potential to achieve these goals. We aimed to identify the linear epitope profile recognized by the serum samples of dengue and Zika patients in the E and NS1 proteins of DENV and ZIKV to select peptides with the potential for the development of diagnostic tests and vaccines. Analysis of a peptide microarray platform with serum samples of dengue and Zika patients demonstrated that the epitopes were evenly distributed across the entire viral proteins, showing no preference for particular regions. However, several epitopes were within epitope hot spots constituted by clusters of peptides recognized in more than 30% of the sub-arrays analyzed with individual or pools of serum samples. The serum samples of dengue and Zika patients showed a high level of cross-reaction for epitopes in the DENV and ZIKV proteins. Analysis of an additional peptide microarray platform containing selected peptides based on the results of the first screening showed that three peptides (DENV: TQGEPSLNEEQDKRF and TQTVGPWHLGKLEID; ZIKV: LELDPPFGDSYIVIG), highly specific for their cognate viruses (p<0.05), were within the epitope hot spots; however, these peptides showed low detection rates (32.5, 35.0, and 28.6%, respectively). We also found two peptides (DENV: WEVEDYGFGVFTTNI and LELDFDLCEGTTVVV) in the epitope hot spots detected by both dengue and Zika patients with similarly high rates (arbitrary detection rate cut-off threshold of ≥40%). The epitope hot spots harbor several immunodominant epitopes recognized by a higher number of individuals when compared to the 15 aa sequence peptides. Therefore, the entire epitope hot spots, spanning up to ~30 aa, would have more potential than peptides of only 15 aa to serve as antigens in diagnostic tests and vaccine developments.
2023-10-11 | GSE235044 | GEO
Project description:Dengue and Zika are two mosquito-borne diseases of great concern, affecting mainly the tropical and subtropical regions worldwide. The arrival of Zika virus (ZIKV) in dengue virus (DENV) endemic areas imposed challenges for differential diagnosis and the development of candidate vaccines. The use of peptides has shown great potential to achieve these goals. We aimed to identify the linear epitope profile recognized by the serum samples of dengue and Zika patients in the E and NS1 proteins of DENV and ZIKV to select peptides with the potential for the development of diagnostic tests and vaccines. Analysis of a peptide microarray platform with serum samples of dengue and Zika patients demonstrated that the epitopes were evenly distributed across the entire viral proteins, showing no preference for particular regions. However, several epitopes were within epitope hot spots constituted by clusters of peptides recognized in more than 30% of the sub-arrays analyzed with individual or pools of serum samples. The serum samples of dengue and Zika patients showed a high level of cross-reaction for epitopes in the DENV and ZIKV proteins. Analysis of an additional peptide microarray platform containing selected peptides based on the results of the first screening showed that three peptides (DENV: TQGEPSLNEEQDKRF and TQTVGPWHLGKLEID; ZIKV: LELDPPFGDSYIVIG), highly specific for their cognate viruses (p<0.05), were within the epitope hot spots; however, these peptides showed low detection rates (32.5, 35.0, and 28.6%, respectively). We also found two peptides (DENV: WEVEDYGFGVFTTNI and LELDFDLCEGTTVVV) in the epitope hot spots detected by both dengue and Zika patients with similarly high rates (arbitrary detection rate cut-off threshold of ≥40%). The epitope hot spots harbor several immunodominant epitopes recognized by a higher number of individuals when compared to the 15 aa sequence peptides. Therefore, the entire epitope hot spots, spanning up to ~30 aa, would have more potential than peptides of only 15 aa to serve as antigens in diagnostic tests and vaccine developments.
2023-10-11 | GSE235043 | GEO