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Transcriptomics coupled proteomics reveals the critical signaling pathways regulating OVA antigen-specific CD8+ T cells in mouse spleen and liver

ABSTRACT: Antigen-specific T cells are particularly important for eliminating bacterial infection, and the dynamics in this process help uncover the mechanisms by which bacteria are eliminated.This study used MHC class I tetramers to recognize the antigen OVA antigen-specific CD8+ T cells in mouse spleen and liver. Then combined the RNAseq and LC-MS/MS analysis to track the changes of the OVA antigen-specific CD8+ T cells at different time points (5 days,7 days, and 14 days post listeria infection).Transcriptomics coupled proteomics reveals the key signaling pathways to regulate antigen-specific CD8+ T cells by infection of Listeria monocytogenes expressing the OVA protein in mouse spleen and liver.

ORGANISM(S): Mus Musculus

SUBMITTER: Jiangbei Yuan

PROVIDER: PXD050970 | iProX | Tue Mar 26 00:00:00 GMT 2024

REPOSITORIES: iProX

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Transcriptomics coupled proteomics reveals the critical signaling pathways regulating OVA antigen-specific CD8+ T cells in mouse spleen and liver

Project description:Background: Antigen-specific T cells are particularly important for eliminating bacterial infection, and the dynamics in this process help uncover the mechanisms by which bacteria are eliminated.Results: In this study, we sorted the antigen-specific CD8+ T cell in the mouse liver and spleen at 5, 7, and 14 days after infection of Listeria monocytogenes expressing the OVA protein, finding that antigen-specific CD8+ T cell expansion after infection peaked on Day 7. Through the RNAseq analysis, we identified 355 genes whose expression peaked on 7 days post-infection shared in both of spleen and liver. For these shared genes, the KEGG pathway analysis showed a notable enrichment in the metabolic pathway. We also discovered 1621 proteins shared in the mouse liver and spleen that peaked seven days after infection by the LC-MS/MS analysis. The KEGG pathway analysis for these proteins revealed a significant enrichment in Splicesome, RNA transport, Ubiquitin mediated proteolysis, and Huntington disease. Transcriptomics coupled proteomics reveals 45 genes/proteins that were elevated on day 7 post listeria infection both in the spleen and liver. These 45 molecules were enriched in Human T-cell leukemia virus 1 infection and T cell activation, which played an important role in the activation of T cells and the anti-infection process.Conclusion: Transcriptomics coupled proteomics reveals the key signaling pathways to regulate antigen-specific CD8+ T cells by infection of Listeria monocytogenes expressing the OVA protein in mouse spleen and liver.

2024-04-10 | GSE263368 | GEO

Expression data from WT and TCF-1-deficient memory CD8 T cells

Project description:TCF-1 is an HMG family transcription factor which is known to be activated by the canonical Wnt signaling pathway and modulated by other signals such as those derived from T cell receptor. We found that during CD8 T cell responses, TCF-1 deficiency impaired long-term maintenance of antigen-specific memory CD8 T cells. We used microarrays to detect gene expression changes in memory CD8 T cells caused by TCF-1 deficiency. Host mice that received WT or TCF-1-deficient OT-I CD8 T cells were infected with attenuated Listeria monocytogenes expressing Ova peptide. In memory phase (i.e., more than 80 days post infection), antigen-specific T cells were ioslated by cell sorting. RNA was extracted and hybridized to GeneChip Mouse GENE 1.0 ST arrays (Affymetrix).

2010-10-04 | E-GEOD-20754 | biostudies-arrayexpress

Hallmarks of CD8 T cell dysfunction are established within hours of tumor antigen encounter

Project description:RNA-SEQ analysis of antigen-specific CD8 T cells sorted from murine liver tumors and from the spleens of Listeria-infected mice at different early timepoints following adoptive transfer. We sequenced naive antigen-specific CD8 T cells from spleens for comparison.

2023-07-10 | GSE209711 | GEO

Hallmarks of CD8 T cell dysfunction are established within hours of tumor antigen encounter

Project description:ATAC-SEQ analysis of antigen-specific CD8 T cells sorted from murine liver tumors and from the spleens of Listeria-infected mice at different early timepoints following adoptive transfer. We sequenced naive antigen-specific CD8 T cells from spleens for comparison. We also sorted tumor-infiltrating antigen-specific CD8 T cells that were removed from tumors and parked in tumor-free hosts for 5 days. The overall goal of this study was to determine the earliest chromatin remodeling events in CD8 T cells activated and differentiating in late tumor-bearing hosts or in infected mice and to determine the extent to which tumor-induced chromatin remodeling was "imprinted."

2023-07-10 | GSE209710 | GEO

Whole genome transcriptome analysis of tumor-specific CD8 T cells in pre-malignant lesions

Project description:Gene expression analysis of tumor-specific CD8 T cells encountering a tumor-specific antigen in pre-malignant lesions in the liver at different time points post tumor initiation. The overall goal of this mouse study was to elucidate the molecular program in tumor-specific T cells encountering a tumor-specific antigen in pre-malignant lesions. The study identifies the genes and pathways that are dysregulated in tumor-specific T cells associated with T cell unresponsiveness in tumors. To identify the genes and pathways that are dysregulated in tumor-specific T cells. Gene signatures of the following sample groups were compared: 1. NaÃ¯ve CD8 T cells; 2. Effector CD8 T cells; 3. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 8-12 days after tumor induction. 4. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 32-34 days after tumor initiation. The mouse tumor model that was used is an autochthonous, tamoxifen-inducible liver cancer model (ASTxCre-ERT2; AST=Albumin-floxStop-SV40 large T antigen; Cre-ERT2 = TAM-dependent Cre-recombinase) in which the SV40 large T antigen serves as the oncogenic driver and tumor-specific antigen; SV40-I TCR transgenic mice, whose CD8 T cells express a Db-restricted TCR specific for the Tag epitope I were used as source of naÃ¯ve tumor-specific CD8 T cells (TCRSV40-I) Total RNA was isolated from flow-sorted transgenic CD8 TCRSV40-I T cells from the following sample groups: NaÃ¯ve, effector, D8-12-pre-malignant lesions, and D32-34 pre-malignant lesions.

2016-08-11 | E-GEOD-60501 | biostudies-arrayexpress

Expression data from MNV-specific CD8 T cells

Project description:Mouse norovirus (MNV) causes acute or chronic infection in immunocompetent hosts, but the CD8 T cell determinants of viral persistence versus clearance are unknown. We used microarrays to interrogate the transcriptional program on MNV-specific CD8 T cells from the spleen and intestine at days 8, 15, 30 post infection with and acute or chronic strain of MNV.

2017-07-24 | GSE101429 | GEO

ATAC-seq of naive and three effector OT-I cell subsets from mice infected with Listeria monocytogenes

Project description:Purpose: ATAC-seq analysis of naive and three effector OT-I cell subsets (from a Klrg1-Cre fate reporter mouse model) isolated from the spleen of C57BL/6 mice 0 and 8 days post infection with OVA-expressing Listeria monocytogenes. The hypothesis tested in the present study was that chromatin remodeling in KLRG1+ effector CD8 T lymphocytes promotes the differentiation into KLRG1- memory CD8 T lymphocytes that provide long-lasting immunity against infectious diseases and malignancies. Methods: DNA was obtained from 50,000 FACS-purified OT-I cell subsets isolated from spleen 0 and 8 days post infection with ovalbumin-expressing Listeria monocytogenes (LM-OVA) (experiment 3). Results: Using ATAC-seq technology, we analyzed the chromatin accessibility landscape of naive and three effector OT-I cells (KLRG1+ Reporter+, KLRG1- Reporter+ (exKLRG1) and KLRG1- Reporter-). Conclusions: Our study represents the first fate mapping analysis of KLRG1+ effector OT-I cells, demonstrates that KLRG1+ effector OT-I cells differentiate into all memory T cell lineages thereby promoting protective immunity. RNA-seq identified CX3CR1 as a marker of circulating exKLRG1 early memory OT-I cells, and ATAC-seq analysis revealed that chromatin remodeling enabled exKLRG1 memory cells to exhibit both a high cytotoxic and proliferative capacity.

2018-03-01 | GSE110876 | GEO

Whole genome transcriptome analysis of tumor-specific CD8 T cells in pre-malignant lesions

Project description:Gene expression analysis of tumor-specific CD8 T cells encountering a tumor-specific antigen in pre-malignant lesions in the liver at different time points post tumor initiation. The overall goal of this mouse study was to elucidate the molecular program in tumor-specific T cells encountering a tumor-specific antigen in pre-malignant lesions. The study identifies the genes and pathways that are dysregulated in tumor-specific T cells associated with T cell unresponsiveness in tumors. To identify the genes and pathways that are dysregulated in tumor-specific T cells. Gene signatures of the following sample groups were compared: 1. Naïve CD8 T cells; 2. Effector CD8 T cells; 3. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 8-12 days after tumor induction. 4. Dysfunctional tumor-specific CD8 T cells isolated from pre-malignant lesions 32-34 days after tumor initiation. The mouse tumor model that was used is an autochthonous, tamoxifen-inducible liver cancer model (ASTxCre-ERT2; AST=Albumin-floxStop-SV40 large T antigen; Cre-ERT2 = TAM-dependent Cre-recombinase) in which the SV40 large T antigen serves as the oncogenic driver and tumor-specific antigen; SV40-I TCR transgenic mice, whose CD8 T cells express a Db-restricted TCR specific for the Tag epitope I were used as source of naïve tumor-specific CD8 T cells (TCRSV40-I)

2016-08-11 | GSE60501 | GEO

Crosstalk between murine marginal zone B cells, macrophages and CD8alpha+ dendritic cells promotes Listeria monocytogenes infection

Project description:Type 1 CD8α+ conventional dendritic cells (cDC1s) harbor and transport Listeria monocytogenes (LM) within the spleen and thereby promote infection; cDC1s are also required for CD8+ T cell priming. To test the role of the second lineage of splenic cDC in regulating infection or adaptive immunity to LM we used Dock8-deficient mice, which have impaired 33D1+ type 2 cDC (cDC2) function. We found reduced CD8+ T cell activation in Dock8-deficient mice, but this was not due to impaired cDC2 function but rather resistance to LM infection. Bacterial resistance was due to loss of marginal zone B (MZB) cells. We showed that IL-10 production by MZB cells did not alter antigen handling pathways in dendritic cells (DCs), including ones relevant for cross-priming or Listeria survival. Instead, IL-10 increased intracellular LM in macrophages in the marginal zone, which transfer bacteria to cDC1s. Bacteria-harboring cDC1s then traffic into the splenic white pulp where protection from sterilizing phagocytes promotes LM expansion. This work uncovers a unique crosstalk between the innate immune cells in the marginal zone, facilitated by IL-10, that promotes both infection but also CD8+ T cell activation.

2019-06-20 | GSE124771 | GEO

miR-17~92 Regulates Effector and Memory CD8 T cell Fates by Modulating Proliferation in Response to Infection

Project description:miRNA profiling of Db-GP33-41 specific murine CD8 T cells following infection with LCMV Armstrong Various in-vivo subsets of antigen-specific CD8 T cells were FACS sorted and analyzed for miRNA expression profiling. Samples were purified from either uninfected animals or after days 4.5, 9 and >60 post infection with LCMV Armstrong.

2013-04-16 | E-GEOD-46052 | biostudies-arrayexpress

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