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RNA-sequencing of bystander-activated memory-like CD4+ T cells

ABSTRACT: RNA-sequencing of bystander-activated memory-like CD4+ T cells

PROVIDER: PRJNA510605 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8349560_1.fastq.gz	Fastqsanger.gz
	SRR8349560_2.fastq.gz	Fastqsanger.gz
	SRR8349561_1.fastq.gz	Fastqsanger.gz
	SRR8349561_2.fastq.gz	Fastqsanger.gz
	SRR8349562_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing of bystander-activated memory-like CD4+ T cells

Project description:We report the differential mRNA expression of memory-like CD4+ T cells stimulated with iL-7, IL-1β, and IL-23. We found memory-like CD4+ T cells stimulated with IL-1β, or with IL-1β and IL-23, in the presence of IL-7, displayed a unique gene expression signature.

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Human CD4+ memory T cells are preferential targets for bystander activation and apoptosis

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Project description:There is much evidence that T cells may be activated via mechanisms which act independently of direct TCR ligation. Despite this, the question of whether such forms of âbystanderâ T cell activation occur during immune responses is hotly debated. To address some outstanding questions, we set up an in vitro system within which to analyse bystander T cell activation in human T cells, in the absence of the possibility for TCR cross-reactivity. In addition, we have investigated the genetic, phenotypic, and functional characteristics of bystander activated T cells. Here, we show that bystander T cell activation is, indeed, observed during a specific immune response, and that it occurs preferentially amongst CD4+ memory T cells. Furthermore, bystander activated T cells display a distinct gene expression profile. The mechanism for bystander T cell activation involves soluble factors, and the outcome is an elevated level of apoptosis. This may provide an explanation for the attrition of T cell memory pools of heterologous specificity during immune responses to pathogens such as viruses. Experiment Overall Design: Three conditions tested with 4 biological repilicates in each: Experiment Overall Design: Resting cells - cells expressing a TCR which does not specifically recognize SEB (VÎ²13.1 T cells) and did not upregulate the activation marker CD25 in response to transwell SEB-stimulated co-culture over a 5 day period. Experiment Overall Design: Bystander activated cells - cells expressing a TCR which does not specifically recognize SEB (VÎ²13.1 T cells), but which did upregulate the activation marker CD25 in response to transwell SEB-stimulated co-culture over a 5 day period. Experiment Overall Design: Directly activated cells - cells expressing a TCR which is known to specifically recognize SEB (VÎ²17 T cells), and which did upregulate the activation marker CD25 in response to direct SEB stimulation over a 5 day period.

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Project description:Gene expression in human activated memory CD4+ T cells

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Gene expression comparing Memory Bystander T cell Function with and without LCMV infection

Project description:We compared the effect of chronic virus infection on the gene expression of memory bystander T cells.

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total RNA-seq from activated CD4-positive, alpha-beta memory T cell (ENCSR694AWV)

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CD4+ cell transcriptional profiling by RNA sequencing

Project description:<p>We use next generation sequencing to investigate the different transcriptomes of closely related CD4+ T-cells from healthy human donors to elucidate the genetic programs that underlie their specialized immune functions. Six cell types were included: Regulatory T-cells (CD25hiCD127low/neg with >95% FOXP3+ purity), regulatory T-cells activated using PMA/ionomycin, CD25-CD45RA+ ('naive' helper T-cells), CD25-CD45RO+ ('memory' helper T-cells), activated Th17 cells (>98% IL17A+ purity) and activated IL17-CD4+ T-cells (called 'ThPI'). Poly-T capture beads were used to isolate mRNA from total RNA, and fragment sizes of ~200 were sequenced from both ends on Illumina's genome analyzer. We confirm many of the canonical signature genes of T-cell populations, but also discover new genes whose expression is limited to specific CD4 T-cell lineages, including long non-coding RNAs. Additionally, we find that genes encoded at loci linked to multiple human autoimmune diseases are enriched for preferential expression upon T-cell activation, suggesting that an aberrant response to T-cell activation is fundamental to pathogenesis.</p>

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