RNA-Seq analysis of Tcf7-deficient and -sufficient lung CD8+ TRM cells after influenza infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA558369 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9892972.fastq.gz | Fastqsanger.gz | |||
| SRR9892973.fastq.gz | Fastqsanger.gz | |||
| SRR9892974.fastq.gz | Fastqsanger.gz | |||
| SRR9892975.fastq.gz | Fastqsanger.gz | |||
| SRR9892976.fastq.gz | Fastqsanger.gz |
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Project description:T cell factor 1 (Tcf1, encoded by Tcf7) promotes the central memory CD8+ T cell (TCM) differentiation and homeostatic proliferation in lymphoid tissues. It remains unclear if and how Tcf1 regulates the CD103high tissue-resident memory CD8+ T cell (TRM) formation in non-lymphoid tissues. Using an influenza A infection mouse model, we collected Tcf7-deficient and -sufficient lung CD8+ TRM cells for RNA sequencing analysis.
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Project description:Lung tissue-resident memory CD8+ T-cells (Trm) are critical for heterosubtypic immunity against influenza virus-(IAV)-reinfection. How these cells surveil the lung, respond to infection and interact with other cells remains unresolved. Here, we used mouse models to identify and enrich lung Trm in combination with intravital and static imaging to assess spatiotemporal dynamics of IAV-induced lung TRM before and after recall-infection. CD69+CD103+ Trm localize to sites of prior influenza infection where they exhibit substantially slower movement properties than non-Trm that also surveil the lung. After rechallenge, lung Trm form tight clusters in an antigen-dependent manner. IAV-specific Trm express several factors that regulate myeloid cell biology and their protective immune responses are accompanied by activation and migration of dendritic cells to draining lymph nodes and recruitment of inflammatory monocytes. Overall, these data reveal the dynamic landscapes of lung Trm cells associated with early protective immunity against IAV infection.
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Project description:The transcription factor Inhibitor of DNA binding 2 (Id2) modulates T cell fate decisions but the molecular mechanism underpinning this regulation is unclear. Here, using whole genome mRNA analysis we show that loss of Id2 programs CD8+ T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. Our findings reveal that the Id2-E2A axis orchestrates T cell differentiation through the induction or repression of downstream transcription factors essential for effector and memory T cell differentiation. Wild-type and Id2fl/flLckCre+ DbNP366-specific CD8+ T cells were isolated from the spleen of PR8-primed/HKx31-infected Ly5.2+Id2fl/flLckCre+:Ly5.1+ mixed bone marrow chimeric mice ten days after intranasal influenza infection and analysed by whole genome mRNA analysis. Three biological replicates of each genotype were subjected to microarray analysis.
2013-05-03 | E-GEOD-44141 | biostudies-arrayexpress
Project description:To evaluate the transcriptional responses of effector and memory virus-specific CD8 T cell subsets after primary and secondary influenza infection, we sorted subsets of FluNP 366-374/Db+ CD8+ T cells from the BAL, lung, and spleen at the peak of primary x31 influenza infection (day 10), resting memory (day 30), or 3 days after secondary PR8 influenza challenge (Day 30+3). Cells from the circulation were excluded from BAL and lung based on intravital labeling with anti-CD45. Memory cells from the lung were further separated in TRM and TEM subsets based on expression of CD69 at the day 30 and day 30+3 timepoints. Memory cells from the BAL were separated into long-term airway resident versus recently-recruited cells based on CD11a expression at the day 30 and days 30+3 timepoints. The results show that virus-specific BAL and lung TRM cells, but not lung TEM cells or spleen TEM cells, rapidly alter their transcriptional program and increase expression of effector molecules within 3 days of a secondary influenza challenge.
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Project description:The precise molecular mechanisms controlling tissue resident T cell (Trm cell) development remain unclear. In our studies, we have found that the vitamin A metabolite all-trans retinoic acid (atRA) synergises with TGFβ to promote Trm cells. We further show that polyclonal activation of naive splenic CD8 T cells in the presense of IL-2, IL-15, TGFβ + atRA leads to the development of CD69+CD103+ Trm cells. We have examined the transcriptome of CD8 T cells under IL-2/15, IL-2/15/atRA, IL-2/IL-15/TGFβ and IL-2/IL-15/TGFβ/atRA conditions.
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Project description:We set out to identify differences in the transcriptome influenced by knockout of the transcription factor T-cell factor 7 (Tcf7) in mouse islets. Furthermore, we wanted to determine if metabolic stress (age,diet) influences these changes. Therefore, we compared the islet transcriptome from WT and Tcf7-/- mice both at a young age (8 weeks old) fed a low fat (10%) diet, versus WT and Tcf7-/- mice at an old age (20 weeks old) on a high-fat (45%) diet. Tcf7-/- mice and littermate wildtype mice were compared. Mice were placed on either a low-fat (10%) or high-fat (45%) diet at weeks of age. For the low fat group, islets from 8 week old mice were isolated and total RNA was extracted with Trizol. For the high fat group, islets from 20 week old mice were isolated and total RNA was extracted with Trizol.
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Project description:Lung resident memory (Trm) CD8 T cells induced by influenza A virus (IAV), are pivotal for providing heterosubtypic immunity, but are not maintained long term, causing gradual loss of protection. This contrasts sharply with long-term maintenance of Trm induced by localized infections of the skin and other tissues. Here we show that the decline in lung Trm is determined by an imbalance between apoptosis and lung recruitment/conversion to Trm of circulating memory cells. At the cellular level, circulating effector memory (Tem) rather than central memory (Tcm) cells are the precursors for conversion to lung Trm. Time-dependent changes in expression of genes critical for Trm differentiation together with enrichment of Tcm diminish the capacity of circulating memory CD8 T cells to form Trm, explaining why IAV-induced Trm are not stably maintained over time. Importantly, systemic booster immunization, through increasing the number of circulating Tem cells, induces an increase in lung Trm pool, providing a new rational for future IAV vaccines.
2016-11-18 | GSE86973 | GEO
Project description:CD8+ TRM are described in autoimmune and chronic inflammatory diseases. However, we still lack knowledge about mechanisms regulating TRM reactivation, in particular in autoimmune diseases. Here, we investigated in a model of TRM-driven central nervous system autoimmunity the transcriptional landscape of self-reactive brain TRM and the requirement of these cells for CD4+ T cell help.
2023-01-25 | GSE189580 | GEO
Project description:Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection. Lung TRM can be generated in response to respiratory infection or vaccination, however, the molecular pathways involved in CD4+TRM establishment have not been defined. Here, we performed transcriptional profiling of influenza-specific lung CD4+TRM following influenza infection to identify pathways implicated in CD4+TRM generation and homeostasis. Lung CD4+TRM displayed a unique transcriptional profile distinct from spleen memory, including up-regulation of a gene network induced by the transcription factor IRF4, a known regulator of effector T cell differentiation.
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Project description:CD8 tissue-resident memory T (TRM) cells provide front-line protection at barrier tissues; however, mechanisms regulating TRM cell development are not completely understood. Priming dictates the migration of effector T cells to the tissue, while factors in the tissue induce in situ TRM cell differentiation. Whether priming also regulates in situ TRM cell differentiation uncoupled from migration is unclear. Here, we demonstrate that T cell priming in the mesenteric lymph nodes (MLN) regulates CD103+ TRM cell differentiation in the intestine. In contrast, T cells primed in the spleen were impaired in the ability to differentiate into CD103+ TRM cells after entry into the intestine. MLN priming initiated a CD103+ TRM cell gene signature and licensed rapid CD103+ TRM cell differentiation in response to factors in the intestine. Licensing was regulated by retinoic acid signaling and primarily driven by factors other than CCR9 expression and CCR9-mediated gut homing. Thus, the MLN is specialized to promote intestinal CD103+ CD8 TRM cell development by licensing in situ differentiation.
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