ScGEX/scTCR-Seq of CD44+ cytotoxic T cells in LCMV-infected Wildtype and Il1rl1-ExAB-/- mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE204693 | GEO | 2023/10/17
REPOSITORIES: GEO
Similar Datasets
Project description:The pleiotropic alarmin interleukin-33 (IL-33) promotes the activity of many innate and adaptive immune cell subsets. Its receptor ST2 is constitutively expressed at high levels by type 2-biased immune cells including CD4+ T helper 2 (Th2) cells, innate lymphoid cells type 2 and highly potent regulatory T cells, allowing rapid sensing of IL-33 alarmin signals (Peine et al., 2015). In contrast, during viral infections, antiviral CD8+ cytotoxic T cells (CTLs) and CD4+ Th1 cells express ST2 at a low level in a transient and activation dependent way, suggesting that the ST2-coding gene Il1rl1 is regulated in a cell-type specific manner (Bonilla et al., 2012). To better understand the transcriptional regulation of the Il1rl1 gene in distinctly polarized T cells, we here performed RNA-Sequencing of in vitro activated, ST2 expressing CTLs, Th1 and Th2 cells. Further, to decipher the T cell subset-specific consequences of IL-33 sensing, we profiled early changes in transcriptional activity of CTLs, Th1 cells and Th2 cells upon stimulation with IL-33. Lastly, to better understand the role of IL-33 during an acute infection with lymphocytic choriomeningitis virus (LCMV), activated CD44+ CTLs were flowcytometrically sorted from infected C57BL/6 wildtype and Il1rl1 gene-targeted mice (Il1rl1-ExAB-/-) and subjected to combined single-cell gene expression and single cell TCR-Seq analysis. This SuperSeries is composed of the SubSeries listed below.
2023-10-17 | GSE204695 | GEO
Project description:To identify the subsets of exhausted T cells and to analyze the transcriptional-metabolic programs alongside their developmental trajectories at single-cell resolution, we isolated CD44+ PD-1hi CD8+ T cells from chronically infected wild-type (WT) mice 21 days after infection with the ‘clone 13’ strain of lymphocytic choriomeningitis virus (LCMV) by FACs sorting aand performed scRNA-sequencing.
2023-09-22 | GSE214003 | GEO
Project description:Gene expression profile in laser-dissected islets of Langerhans in the inducible RIP-LCMV-GP mouse model for type 1 diabetes (T1D) RIP-LCMV-GP mice express the glycoprotein (GP) of the lymphocytic choriomeningitis virus (LCMV) in the beta-cells (rat insulin promotor, RIP); T1D develops 10-14 after LCMV-infection
2023-10-01 | GSE229287 | GEO
Project description:Investigation of the change of the Trail-dependent NK cell transcriptome during short-term (24h) infection with lymphocytic choriomeningitis virus (LCMV). RNA sequencing-based transcriptomics analysis was performed in spleen-isolated (NK1.1+CD3-) NK cells from 3 naïve Trail+/+ mice, 3 naive Trail-/- mice, 4 LCMV-infected Trail+/+ mice, and 4 LCMV-infected Trail-/- mice.
2019-08-27 | E-MTAB-7562 | biostudies-arrayexpress
Project description:Lymphocytic Choriomeningitis Virus (LCMV) specific CD8+ T cells (P14) were transferred into congenic WT mice followed by LCMV(DOCILE) infection. CXCR5-expressing (CXCR5+) or CXCR5 non-expressing (CXCR5-) P14 were purified on day 8 after infection, and total mRNA were sequenced from these populations. mRNA of P14 from uninfected mice (Naive P14) was also sequenced. Examination of mRNA level in CXCR5 expressing P14 (CXCR5+P14) and non-expressing P14 (CXCR5-P14) from LCMV infected mice day 8 post infection. mRNA of P14 from uninfected mice (Naïve P14) was also examined.
2016-07-31 | E-GEOD-76279 | biostudies-arrayexpress
Project description:Lymphocytic Choriomeningitis Virus (LCMV) specific CD8+ T cells (P14) were transferred into congenic WT mice followed by LCMV(DOCILE) infection. CXCR5-expressing (CXCR5+) or CXCR5 non-expressing (CXCR5-) P14 were purified on day 8 after infection, and total mRNA were sequenced from these populations. mRNA of P14 from uninfected mice (Naive P14) was also sequenced.
2016-07-31 | GSE76279 | GEO
Project description:Myeloid-derived suppressor cells (MDSC) are major negative regulators of immune responses in cancer and chronic infections. It remains unclear if regulation of MDSC activity at different conditions is controlled by similar mechanisms. In order to compare MDSC in mice with cancer and lymphocytic choriomeningitis virus (LCMV) infection, we would like to perform gene profiling and comparison of M-MDSCs in tumor bearing and LCMV infected mice using total RNAseq:
2021-08-02 | GSE179278 | GEO
Project description:To determine the effects of excess IL-18 on virus-induced immunopathology, we infected Il18-transgenic (Il18tg) mice with Lymphocytic Choriomeningitis Virus (LCMV, Armstrong). LCMV infection is self-limited in wild-type (WT) mice, but Prf1-/- mice develop prolonged viremia and fatal HLH. LCMV-infected Il18-transgenic (Il18tg) mice developed cachexia and hyperinflammation comparable to Prf1-/- mice, albeit with minimal mortality. We use RNA-sequencing to identify differences in the transcriptome of GP33 - specific CD8 T cells from these mice in comparison to a wild type mouse under the same conditions. We saw expression of Ifng was elevated about 4-fold in both Prf1-/- and Il18tg mice. Genes specifically upregulated in Il18tg CD8 T-cells included Csf2, Il1rl1, and Il12rb2. We also saw differences between Prf1-/- and WT/Il18tg CD8 T-cells that included Klrg1 and transcripts associated with CD8 T-cell exhaustion, including the inhibitory receptors Lag3, Havcr2, and Tigit, and the transcription factors Tox and Prdm1. These data support that IL-18 as a potent, independent, and modifiable driver of life-threatening innate and adaptive hyperinflammation, and support the rationale for an IL-18-driven subclass of hyperinflammation.
2020-11-12 | GSE150077 | GEO
Project description:CD4 T cells promote innate and adaptive immune responses, but how vaccine-elicited CD4 T cells contribute to immune protection remains unclear. Here we evaluated whether induction of virus-specific CD4 T cells by vaccination would protect mice against infection with chronic lymphocytic choriomeningitis virus (LCMV). Immunization with vaccines that selectively induced CD4 T cell responses resulted in catastrophic inflammation and mortality following challenge with a persistent form of LCMV. Immunopathology required antigen-specific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-organ system failure. Virus-specific CD8 T cells or antibodies abrogated the pathology. These data demonstrate that vaccine-elicited CD4 T cells in the absence of effective antiviral immune responses can trigger lethal immunopathology. Splenic GP66-specific CD4 T cells from mice immunized with either a LMwt vaccine (sham) or LMgp61 vaccine (CD4 vaccine) were purified by FACS on day 8 post-infection with LCMV clone 13
2014-12-04 | E-GEOD-63825 | biostudies-arrayexpress
Project description:Metabolic and nutrient-sensing pathways play an important role in controlling the efficacy of effector T cells. Oxygen is a critical regulator of cellular metabolism. However, during immune responses T cells must function in oxygen-deficient, or hypoxic, environments. Here, we used high resolution mass spectrometry to investigate how hypoxia configures the proteome of CD8+ cytotoxic T lymphocytes (CTLs). We identified and quantified over 7,600 proteins and discovered that hypoxia increased the abundance of a selected number of proteins in CTLs. This included glucose transporters, metabolic enzymes, transcription factors, cytolytic effector molecules, checkpoint receptors and adhesion molecules. While some of these proteins may augment the effector functions of CTLs, others may limit their cytotoxicity. These data provide a comprehensive resource for understanding the magnitude of the CTL response to hypoxia and emphasise the importance of oxygen-sensing pathways for controlling CD8+ T cells. Additionally, this study provides new understanding about how hypoxia may promote the effector function of CTLs, while contributing to their dysfunction in some contexts. For this project, P14 cytotoxic T cells (CTLs) were generated from T cells from the spleens of mice. CD8+ T cells were activated for 2 days with the P14-T cell receptor (TCR) cognate ligand (peptide gp33-41 from Lymphocytic Choriomeningitis Virus, LCMV) in the presence of 20 ng/ml IL 2 (Proleukin) and 2 ng/ml IL-12 (Peprotech). Cells were grown in a humidified incubator with a gas atmosphere of 18% oxygen and 5% CO2 and a temperature of 37�C. After 48 hours, the activated CD8+ T cells were removed from TCR stimulation and were cultured in RPMI 1640, with 10% foetal bovine serum (FBS), supplemented with 100 units/ml penicillin-G, 100 �g/ml streptomycin, 50 �M-mercaptoethanol and 20 ng/ml IL-2 (Proleukin). Each day, the T cells were counted and split to 500,000 cells per ml with fresh IL-2 being added to a final concentration of 20 ng/ml. CTLs were differentiated in IL-2 for 4 days, before being counted and re-suspended at a concentration of 300,000 cells per ml in RPMI with 10% foetal bovine serum, 50 units/ml penicillin-G, 50 �g/ml streptomycin, 50 �M-mercaptoethanol and 20 ng/ml IL-2. A volume of 8 mls of the cell suspension was plated per well of a 6 well plate, and the CTLs were either maintained in a gas atmosphere of 18% oxygen and 5% CO2 or transferred to an atmosphere of 1% O2 and 5% CO2 in a Galaxy 48 R incubator (Eppendorf) for 24 hours. Three biological replicates (CTLs generated from three separate spleens) were analysed in this experiment."
2021-10-20 | PXD026223 | Pride