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

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

PROVIDER: PRJNA798252 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17652343_1.fastq.gz	Fastqsanger.gz
	SRR17652343_2.fastq.gz	Fastqsanger.gz
	SRR17652344_1.fastq.gz	Fastqsanger.gz
	SRR17652344_2.fastq.gz	Fastqsanger.gz
	SRR17652345_1.fastq.gz	Fastqsanger.gz

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Transcription profiling of human PBMC treated with anti-CD25 mAb

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. Experiment Overall Design: Peripheral blood mononuclear cells (PBMC) were stimulated for 8 or 16 hrs with 100 ng/ml OKT-3 together with 100 U/ml recombinant human interleukin-2 (rhIL-2) in the absence or presence of 30 Âµg/ml anti-CD25 antibody. RNA from cells under such treatment was isolated with Trizol and subjected to microarray analysis onto human U133A microarray following the Affymetrix protocol.

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

Project description: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.

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Expression data from human peripheral blood lymphocytes stimulated with anti-CD3 and anti-CD28 antibodies.

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

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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

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