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Effect of BTK and GSK3 inhibition on gene expression in primary peripheral human B cells

ABSTRACT: Effect of BTK and GSK3 inhibition on gene expression in primary peripheral human B cells

PROVIDER: PRJNA848850 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19645629_1.fastq.gz	Fastqsanger.gz
	SRR19645629_2.fastq.gz	Fastqsanger.gz
	SRR19645630_1.fastq.gz	Fastqsanger.gz
	SRR19645630_2.fastq.gz	Fastqsanger.gz
	SRR19645631_1.fastq.gz	Fastqsanger.gz

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Effect of BTK and GSK3 inhibition on gene expression in primary peripheral human B cells

Project description:To investigate the BTK and GSK3 in the regulation of human B cell biology, we treated B cells from peripheral blood with either vehicle or BTK inhibitor or GSK3 in presence or absence of BCR cross-linking antibodies. We then performed gene expression profiling analysis using data obtained from RNA-seq of those samples at 24hrs.

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Modeling the clinical phenotype of BTK inhibition in the mature murine immune system

Project description:Using the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice autoimmune indications. However, our current knowledge of the role of BTK in immune competence has been gathered in the context of genetic inactivation of btk in both mice and man. Using the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice. We implicate BTK in tonic BCR signaling, demonstrate dependence of the T3 B cell subset and IgM surface expression on BTK activity, and find that B1 cells survive and function independently of BTK. While BTK inhibition does not impact humoral memory survival, antigen-driven clonal expansion of memory B cells and antibody secreting cell generation are inhibited. These data define the role of BTK in the mature immune system and mechanistically predict the clinical phenotype of BTK inhibition. We used Affymetrix genechips to profile the transcriptional changes downstream of BTK inhibition after in vivo B-cell activation by anti-IgD Mice were injected with the novel BTK inhibitor PF-303 2 hours prior to anti-IgD mediated in vivo B-cell activation; B-cells where harvested 2 hours after anti-IgD activation and RNA isolated.

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