Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The impact of TCR affinity on resident memory T cell formation during influenza virus infection

ABSTRACT: The impact of TCR affinity on resident memory T cell formation during influenza virus infection

PROVIDER: PRJNA540769 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9002450.fastq.gz	Fastqsanger.gz
	SRR9002451.fastq.gz	Fastqsanger.gz
	SRR9002452.fastq.gz	Fastqsanger.gz
	SRR9002453.fastq.gz	Fastqsanger.gz
	SRR9002454.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

The impact of TCR affinity on resident memory T cell formation during influenza virus infection

Project description:Resident memory T (TRM) cells in the lung are vital for heterologous protection against influenza A virus (IAV). Environmental factors are necessary to establish lung TRM, however the role of T cell intrinsic factors like T cell receptor (TCR) signal strength have not been elucidated. Here we investigated the impact of TCR signal strength on the generation and maintenance of lung TRM cells after IAV infection. We inserted high and low affinity OT-I epitopes into IAV and infected mice after transfer of OT-I T cells. We uncovered a bias in TRM formation in the lung elicited by lower affinity TCR stimulation. TCR affinity did not impact the overall phenotype or long-term maintenance of lung TRM cells. Overall, these findings demonstrate that TRM formation is negatively correlated with increased TCR signal strength. Lower affinity cells may have an advantage in forming TRM to ensure diversity in the antigen-specific repertoire in tissues.

2019-06-18 | GSE130609 | GEO

The Impact of TCR Signal Strength on Resident Memory T Cell Formation during Influenza Virus Infection.

Project description:Resident memory T cells (TRM) in the lung are vital for heterologous protection against influenza A virus (IAV). Environmental factors are necessary to establish lung TRM; however, the role of T cell-intrinsic factors like TCR signal strength have not been elucidated. In this study, we investigated the impact of TCR signal strength on the generation and maintenance of lung TRM after IAV infection. We inserted high- and low-affinity OT-I epitopes into IAV and infected mice after transfer of OT-I T cells. We uncovered a bias in TRM formation in the lung elicited by lower affinity TCR stimulation. TCR affinity did not impact the overall phenotype or long-term maintenance of lung TRM Overall, these findings demonstrate that TRM formation is negatively correlated with increased TCR signal strength. Lower affinity cells may have an advantage in forming TRM to ensure diversity in the Ag-specific repertoire in tissues.

| S-EPMC6684852 | biostudies-literature

Transcriptional profiling of OT-1 cells during in vitro memory formation after high- or low-affinity priming

Project description:To understand the impact of TCR affinity during priming on memory formation, we performed transcriptional profiling of OT-1 cells at different time points after stimulation with high- or low-affinity ligands. Our findings indicate that low-affinity stimulaation is associated with earlier memory formation.

2020-01-06 | GSE102189 | GEO

TCR affinity defines tumor-specific CD8 T cell differentiation and dysfunction [RNA-seq]

Project description:RNA-seq analysis of tumor-specific CD8 T cells encountering tumor antigens with varying TCR/pMHC affinity.

2021-12-11 | GSE141817 | GEO

Affinity and Dose of TCR Engagement Yield Proportional Enhancer and Gene Activity in CD4+ T Cells

Project description:Affinity and dose of T cell receptor (TCR) interaction with antigens govern the magnitude of CD4+ T cell responses, but questions remain regarding the quantitative translation of TCR engagement into downstream signals. We find that while the response of CD4+ T cells to antigenic stimulation is bimodal, activated cells exhibit analog responses proportional to signal strength. Gene expression output reflects TCR signal strength, providing a signature of T cell activation. Expression changes rely on a pre-established enhancer landscape and quantitative acetylation at AP-1 binding sites. Finally, we show that graded expression of activation genes depends on ERK pathway activation, suggesting that an ERK-AP-1 axis translates TCR signal strength into proportional activation of enhancers and genes essential for T cell function. CD4+ T cells from transgenic AND mice were sequenced under the conditions indicated. Replicates are included for each type of data (RNA-Seq, ChIP-Seq), and are numbered accordingly. The No Peptide condition serves as the untreated control for the peptide-treated samples, and inputs are provided for ChIP-Sequencing samples.

2016-06-01 | E-GEOD-69545 | biostudies-arrayexpress

T cell receptor signal strength and antigen affinity differentially regulate memory CD8+ T cell development

Project description:IL-2 inducible tyrosine kinase (Itk) is a Tec family non-receptor tyrosine kinase that is known to regulate T cell receptor signal strength (TcR) and T cell development and differentiation. TcR signal strength and antigen affinity are parameters known to regulate the development of CD8+ T cell memory. However, the intersection between TcR signal strength and antigen affinity on CD8+ memory T cell development remains unclear. Therefore, we compared the transcriptomes of WT and Itk-/- OT-1/Rag-/- CD8+ T cells at day 0 and day 7 following infection with Listeria monocytogenes expressing the SIINFEKL (N4) or SIITFEKL (T4) OVA peptide variant (different affinities for TcR) by RNA sequencing.

2020-09-30 | GSE137406 | GEO

Zfp36l1 establishes the high affinity CD8 T cell response by directly linking TCR affinity to cytokine sensing

Project description:The T cell effector phase is dominated by few T cells with high affinity TCR for the respective immunodominant antigen. During priming T cells have to process multiple cues in form of antigen, costimulation and cytokines, thus a plethora of T cells with different specificities and affinities has to compete for these cues. IL2 has been suggested to be a pivotal pleiotropic molecule which organizes the quantity, quality and clonal composition of T cells contributing to the effector response. How individual T cells compete for and respond to IL2 and other key cytokines at the molecular level and as a consequence, how this competition shapes population dynamics is still poorly understood. Here we describe how the RNA binding protein ZFP36L1 acts as a sensor of antigen affinity and establishes dominance of high affinity T cells by promoting the response to IL2.

2023-04-24 | GSE230373 | GEO

Gene expression of early memory and effector precursor CD8 T cells generated by differential TCR signaling strength

Project description:Asymmetric cell division (ACD) and the strength of initial T cell receptor (TCR) signaling are both implied to contribute to the establishment of cellular heterogeneity and CD8 T cell effector and memory differentiation. However, on a single cell level it remained unclear whether ACD generates progeny of different fates and whether the strength of TCR signaling affects this mechanism. Therefore, we developed experimental systems allowing monitoring the fate of single daughter cell progenies derived from an ACD either induced by weak or strong TCR stimulation by in vitro live imaging. We used the combinatorial expression of TCF1 and CD62L as markers indicating fate specification a few days after activation and analyzed the transcriptional profiles of in vitro generated CD62L+TCF1+ and CD62L-TCF1- cells derived from either antibody-induced (AB) activation or from gp33 (high affinity) or C6 (low affinity) peptide stimulation and compared them to in vivo generated effector and memory cells, respectively. Therefore, we sorted CD62L+TCF1+ and CD62L-TCF1- cells on day 6 post activation, followed by bulk RNA sequencing and found that CD62L+TCF1+ cells transcriptionally resembled in vivo generated memory cells, whereas CD62L-TCF1- cells were similar to in vivo generated effector cells.

2023-02-17 | E-MTAB-12563 | biostudies-arrayexpress

TCR affinity defines tumor-specific CD8 T cell differentiation and dysfunction

Project description:TCR affinity defines tumor-specific CD8 T cell differentiation and dysfunction

| PRJNA594907 | ENA

Affinity and Dose of TCR Engagement Yield Proportional Enhancer and Gene Activity in CD4+ T Cells

2016-06-01 | GSE69545 | GEO