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IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

ABSTRACT: IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

PROVIDER: PRJNA860292 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20307475.fastq.gz	Fastqsanger.gz
	SRR20307476.fastq.gz	Fastqsanger.gz
	SRR20307477.fastq.gz	Fastqsanger.gz
	SRR20307478.fastq.gz	Fastqsanger.gz
	SRR20307479.fastq.gz	Fastqsanger.gz

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Similar Datasets

IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

Project description:IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

| PRJNA935745 | ENA

IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

Project description:To investigate IL-21 producing CD4 T cells, we infected IL21-VFP reporter mice with mouse polyomavirus and compared VFP+ (IL-21+) CD4 T cells to VFP- (IL-21-) CD4 T cells in the brains and spleens.

2023-02-16 | GSE225462 | GEO

IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection

Project description:To investigate the effect of interleukin (IL)-21 signaling on CD8 T cells and compare IL21-receptor deficient CD8 T cells to CD8 T cells derived from CD4 T cell deficient mice, we infected IL21-receptor knock-out mice, CD4 T cell depleted mice, and wild-type mice intracranially with Mouse Polyomavirus. We then performed gene expression profiling analysis using data obtained from RNA-seq of CD8 T cells derived from the brains of the mice at 30 day post infection.

2022-07-22 | GSE208537 | GEO

IL-21 from high-affinity CD4 T cells drives differentiation of brain-resident CD8 T cells during persistent viral infection.

Project description:Development of tissue-resident memory (TRM) CD8 T cells depends on CD4 T cells. In polyomavirus central nervous system infection, brain CXCR5hi PD-1hi CD4 T cells produce interleukin-21 (IL-21), and CD8 T cells lacking IL-21 receptors (IL21R-/-) fail to become bTRM IL-21+ CD4 T cells exhibit elevated T cell receptor (TCR) affinity and higher TCR density. IL21R-/- brain CD8 T cells do not express CD103, depend on vascular CD8 T cells for maintenance, are antigen recall defective, and lack TRM core signature genes. CD4 T cell-deficient and IL21R-/- brain CD8 T cells show similar deficiencies in expression of genes for oxidative metabolism, and intrathecal delivery of IL-21 to CD4 T cell-depleted mice restores expression of electron transport genes in CD8 T cells to wild-type levels. Thus, high-affinity CXCR5hi PD-1hi CD4 T cells in the brain produce IL-21, which drives CD8 bTRM differentiation in response to a persistent viral infection.

| S-EPMC7721466 | biostudies-literature

Resident memory T cells form during persistent antigen exposure leading to allograft rejection

Project description:Resident memory T cells form during persistent antigen exposure leading to allograft rejection

| PRJNA699537 | ENA

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

IL-21 in Homeostasis of Resident Memory and Exhausted CD8 T Cells during Persistent Infection.

Project description:CD4 T cells guide the development of CD8 T cells into memory by elaborating mitogenic and differentiation factors and by licensing professional antigen-presenting cells. CD4 T cells also act to stave off CD8 T cell dysfunction during repetitive antigen stimulation in persistent infection and cancer by mitigating generation of exhausted T cells (TEX). CD4 T cell help is also required for establishing and maintaining tissue-resident memory T cells (TRM), the nonrecirculating memory T cell subset parked in nonlymphoid tissues to provide frontline defense against reinvading pathogens. Interleukin (IL)-21 is the signature cytokine secreted by follicular helper CD4 T cells (TFH) to drive B cell expansion and differentiation in germinal centers to mount high-affinity, isotype class-switched antibodies. In several infection models, IL-21 has been identified as the CD4 T help needed for formation and survival of TRM and TEX. In this review, we will explore the different memory subsets of CD8 T cells in persistent infections, the metabolic profiles associated with each, and evidence documenting the importance of CD4 T cell-derived IL-21 in regulating CD8 TRM and TEX development, homeostasis, and function.

| S-EPMC7554897 | biostudies-literature

Heart-resident PDGFRa+ SCA-1+ cells

Project description:Heart-resident PDGFRa+ SCA-1+ cells

| PRJNA595180 | ENA

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

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

| PRJNA540769 | ENA

Resident memory T cells form during persistent antigen exposure leading to allograft rejection

Project description:Tissue resident memory T cells (TRM) contained at sites of previous infection provide local protection against re-infection. Whether they form and function in organ transplants where cognate antigen persists is unclear. This is a key question in transplantation as T cells are detected long-term in allografts, but it is not known whether they are exhausted or are functional memory T cells. Using a mouse model of kidney transplantation, we showed that antigen-specific and polyclonal effector T cells differentiated in the graft into TRM and subqeuntly caused allograft rejection. TRM identity was established by surface phenotype, transcriptional profile, and inability to recirculate in parabiosis and re-transplantation experiments. Graft TRM proliferated locally, produced IFNγ upon re-stimulation, and their in vivo depletion attenuated rejection. Importantly, the vast majority of antigen-specific and polyclonal TRM lacked phenotypic and transcriptional exhaustion markers. Single cell analysis of graft T cells early and late after transplantation identified a transcriptional program associated with transition to the tissue resident state that could serve as a platform for the discovery of therapeutic targets. Thus, recipient effector T cells differentiate into functional graft TRM that maintain rejection locally. Targeting these TRM could improve renal transplant outcomes.

2021-03-20 | GSE166166 | GEO

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