Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from peripheral human T cells stimulated with an anti-CD96 mAb

ABSTRACT: The role of CD96 in human T cells is ambiguous. We demonstrated that engagement of CD96 on human T cells by antibodies provides a strong activating signal dependent on antibody isotype and cross-linking by a subset of Fcγ receptors. Here we used RNASeq profiling to analyze the gene expression programme associated with anti-CD96 mAb treatment in purified T cells isolated from the blood of healthy donors. We showed that multiple hallmarks associated with an activated T-cell signature were significantly enriched in the anti-CD96 treatment group. These included gene signatures associated with cell cycle progression, metabolic reprogramming, effector differentiation, and sustained proliferation and survival. Using pathway analysis, we identified several candidate molecules that could mediate signaling downstream of CD96.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193864 | GEO | 2022/09/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptomic data of B-cell lymphoma bearing mice treated with anti-CD20/-CD27 mAb therapy

Project description:We report the single-cell RNA sequencing data obtained from BCL1 lymphoma-bearing mice treated with either isotype control, anti-CD20 mAb, anti-CD27 mAb or anti-CD20+anti-CD27 mAb together

2018-01-12 | GSE97037 | GEO

Expression analysis of primary human monocytes stimulated with an anti-TLR10 mAb (5C2C5)

Project description:We report that engagment of TLR10 via the 5C2C5 anti-TLR10 mAb causes differential expression is a subset of inflammatory, miRNA and uncharacterized genes compared to an isotype control antibody

2017-02-17 | GSE94969 | GEO

Expression profiles of TREM-1 high and TREM-1 low expressing monocytes

Project description:The expression of Triggering Receptor Expressed on Myeloid cells (TREM)-1 has been described as a predictive marker for anti-Tumor Necrosis Factor (TNF)-α monoclonal antibody (mAb) therapy responsiveness in patients with inflammatory bowel disease (IBD). Here we investigated expression of TREM-1 specifically in CD14+ monocytes in relation to anti-TNF response. The pretreatment TREM-1 expression levels of CD14+ monocytes of Crohn’s disease (CD) patients were predictive of outcome to anti-TNF mAb therapy, with low TREM-1 expression associated with response to anti-TNF. FACSorting of CD14+ monocytes with different TREM-1 levels showed that differentiation towards regulatory CD206+ M2 type macrophages by anti-TNF was suppressed in CD14+ monocytes with high TREM-1 expression. Activity of the Fcγ-Receptor and autophagy pathway, both necessary for M2 type differentiation and the response to anti-TNF, were decreased in CD14+ monocytes with high expression of TREM-1. We confirmed that the activity of the Fcγ-Receptor pathway was decreased in the CD patients that did not respond to anti-TNF therapy and that it was negatively correlated with TREM-1 expression levels in the CD patient cohort. In conclusion, our results indicate that TREM-1 expression levels in CD14+ monocytes associate with decreased autophagy and FcγR activity resulting in decreased differentiation to M2 type regulatory macrophages upon anti-TNF mAb treatment, which may explain anti-TNF non-response in IBD patients with high expression levels of TREM-1.

2021-04-07 | GSE165522 | GEO

Influence of anti-CD25 mAb on the transcriptome of activated PBMC

Project description:CD25 monoclonal antibody binding to the alpha-chain of the Interleukin-2 (IL-2) receptor, blocks high affinity IL-2 binding thereby preventing complete T cell activation and being of ample importance in transplantation medicine and potentially the treatment of autoimmune disease. However, CD25 antibodies do not only block T cell activation but also prevent activation induced cell death (AICD) attributing a dual function to IL-2. In this study, the modulation of the genomic expression profile of human peripheral blood mononuclear cells (PBMC) with therapeutic concentrations of humanized anti-CD25 mAb was investigated. PBMC were stimulated with CD3 antibody OKT-3 together with recombinant IL-2 in the absence or presence of anti-CD25 mAb. RNA was extracted and subjected to microarray analysis on U133A microarrays (Affymetrix). The expression profile revealed the up-regulation of 62 genes and down-regulation of 38 genes by anti-CD25 mAb, respectively.

2009-05-02 | GSE15928 | GEO

Transcription profiling of human PBMC treated with anti-CD25 mAb

2009-05-11 | E-GEOD-15928 | biostudies-arrayexpress

Blockade of the neogenin-RGMb-BMP signaling hub inhibits allergen-induced airway hyperreactivtiy

Project description:Bronchial asthma is associated with type 2 immune responses induced by components of adaptive as well as innate immunity. Although innate cytokines such as IL-25 have been shown to play key roles in development of airway hyperreactivity (AHR), little is known of innate molecules that regulate IL-25-mediated airway inflammation. We found that blockade of repulsive guidance molecule b (RGMb) in an experimental murine model of asthma blocked the development of AHR, a cardinal feature of asthma, and that RGMb is expressed on F4/80+CD11b+CD11cneg macrophages (RGMb+ macrophages), which accumulated in the lungs of OVA-sensitized and challenged mice, but not in naÃ¯ve mice. Moreover, we found that a large fraction of the RGMb+ macrophages expressed the IL-25 receptor IL-17RB and produced IL-13. IL-25 was critical for the development of AHR in our model, since mice deficient in IL-17RB did not develop AHR. Finally, treatment with anti-RGMb mAb during the challenge phase of the protocol after allergen sensitization effectively prevented the development of AHR and airway inflammation, suggesting for the first time that RGMb+ cells, including RGMb+ macrophages, play critical roles in allergen-induced asthma. We used microarrays to compare the gene expression patterns in WT mice sensitized and challenged with OVA that were treated with either RGMb mAb or an isotype control. First replicate: 3 control samples (mice sensitized and challenged with saline), 3 RGMb mAb samples, 3 isotype samples; 2nd replicate: 3 control samples, 3 RGMb mAb samples, 2 isotype samples. Lung tissues were harvested at the same treatment time point in all groups.

2016-03-14 | E-GEOD-79156 | biostudies-arrayexpress

Identification of transcription factor MAB-5 binding sites

Project description:We identified the DNA binding sites of MAB-5 in C. elegans. MAB-5 was C-terminally tagged with GFP and the expression pattern was examined through fluorescent microscopy. The binding sites were determined using chromatin immunoprecipitation with anti-GFP antibody followed by illumina high-throughput sequencing (ChIP-seq). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Identification of MAB-5 binding sites at L3 stage

2009-04-11 | E-GEOD-15625 | biostudies-arrayexpress

Identification of transcription factor MAB-5 binding sites

2009-04-11 | GSE15625 | GEO

The effect of ANGPTL3 mAb on liver transcriptomes in LDLR-deficient mice

Project description:Purpose: The goal of this study was to evaluate the effect of ANGPTL3 inhibition on liver transcriptomes in LDLR KO mice. Methods: Mice were treated once weekly for 3 weeks with 25mg/kg control mAb or ANGPTL3 mAb. Livers were harvested 6 days after the last mAb treatment. Results: ANGPTL3 inhibition had no major impact on hepatic gene expression.

2020-07-05 | GSE143726 | GEO

Norepinephrine inhibits CD8+ T cell infiltration and function, inducing anti-PD-1 mAb resistance in lung adenocarcinoma

Project description:BACKGROUND:Mental stress-induced neurotransmitters can affect the immune system in various ways, leading to tumor immune escape. Therefore, a better understanding of the potential functions of neurotransmitters in the tumor immune microenvironment is expected to promote the development of novel anti-tumor therapies, while facilitating synergistic immune therapy. METHODS: In this study, we analyzed the plasma levels of neurotransmitters in anti-programmed cell death protein 1 (PD-1) monoclonal antibody (mAb)-resistance patients and sensitive patients, to identify significantly different neurotransmitters. Subsequently, animal experiments, transcriptome analysis, metabolomic analysis, and experiments in vitro were used to reveal the specific mechanism of norepinephrine’s (NE) effect on immunotherapy. RESULTS: The plasma NE levels were higher in anti-PD-1 mAb-resistance patients, which may be the main cause of anti-PD-1 mAb resistance. An animal model was established for verification, which further demonstrated that NE could cause anti-PD-1 mAb resistance. Then, from the perspective of the immunosuppressive microenvironment to explore the specific mechanism of NE-induced anti-PD-1 mAb resistance, we found that NE can affect the secretion of the C-X-C Motif Chemokine Ligand 9 (CXCL9) and the immunosuppressive metabolite adenosine (ADO) in tumor cells, thereby inhibiting chemotaxis and function of CD8+ T cells. Notably, the WNT7A/β-catenin signaling pathway plays a crucial role in the NE-induced decrease in the secretion of CXCL9 and disturbance of ADO metabolism. CONCLUSION: NE can affect the secretion of CXCL9 and ADO in tumor cells, thereby inhibiting chemotaxis and the function of CD8+ T cells and inducing anti-PD-1 mAb resistance in lung adenocarcinoma (LUAD).

2023-04-04 | GSE218402 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data