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ScGEX/scTCR-Seq of CD44+ cytotoxic T cells in LCMV-infected Wildtype and Il1rl1-ExAB-/- mice

ABSTRACT: To study the effect of IL-33 sensing on CD8 T cell differentiation during 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE204693 | GEO | 2023/10/17

REPOSITORIES: GEO

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scGEX/scTCR-Seq of CD44+ cytotoxic T cells in LCMV-infected Wildtype and Il1rl1-ExAB-/- mice

Project description:scGEX/scTCR-Seq of CD44+ cytotoxic T cells in LCMV-infected Wildtype and Il1rl1-ExAB-/- mice

| PRJNA841968 | ENA

A type 1 immunity-restricted promoter of the IL-33 receptor gene drives antiviral T cell responses

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

Single cell sequecing analysis of exhausted CD8 T cell subsets in LCMV-clone13 infected mice

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

Gene expression in diabetic RIP-LCMV-GP mice

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

Comparison of Trail+/+ versus Trail-/- splenic NK cells from naïve and LCMV-infected mice

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

CXCR5+ Follicular Cytotoxic T cells Control Viral Infection in B Cell follicles

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 (NaÃ¯ve P14) was also examined.

2016-07-31 | E-GEOD-76279 | biostudies-arrayexpress

CXCR5+ Follicular Cytotoxic T cells Control Viral Infection in B Cell follicles

2016-07-31 | GSE76279 | GEO

Total RNAseq of fixed M-MDSC isolated from tumor bearing and LCMV infected mice

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

Interleukin-18 and cytotoxic impairment are independent and synergistic causes virus-induced hyperinflammation in mice

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

Vaccine-Elicited CD4 T Cells Induce Immunopathology Following Chronic LCMV Infection

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

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