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Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scRNA-Seq]

ABSTRACT: Longitudinal scRNA-seq from LCMV-specific P14 CD8 T cells in LCMV-Armstrong and LCMV-Clone 13 infection

ORGANISM(S): Mus musculus

PROVIDER: GSE199563 | GEO | 2022/10/31

REPOSITORIES: GEO

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Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scATAC-Seq 2]

Project description:Longitudinal scATAC-seq from LCMV-specific P14 CD8 T cells in LCMV-Armstrong and LCMV-Clone 13 infection

2022-10-31 | GSE199557 | GEO

Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scRNA-seq and scATAC-seq coAssay]

Project description:Longitudinal scRNA-seq and scATAC-seq from LCMV-specific P14 CD8 T cells in LCMV-Armstrong and LCMV-Clone 13 infection

2023-05-31 | GSE230363 | GEO

Longitudinal single cell transcriptional and epigenetic mapping of effector, memory, and exhausted CD8 T cells reveals shared biological circuits across distinct cell fates [scATAC-Seq 1]

Project description:scATAC-seq from LCMV-specific P14 CD8 T cells after LCMV-Armstrong at day 60 and day 200 post infection

2022-10-31 | GSE199556 | GEO

Tox reinforces the phenotype and longevity of exhausted T-cells in chronic viral infection [day 8 acute vs chronic]

Project description:Chronic CD8 T-cell stimulation in persisting infections or tumors can induce a stable gene expression program, known as T-cell dysfunction or exhaustion, that limits the cell’s effector functions and anti-viral and anti-tumor immunity. Thus far, the underlaying molecular mechanisms that induce and stabilize this phenotype are vaguely understood. We report here that establishing this program requires the thymocyte selection-associated high mobility group-box protein (Tox). Genetic disruption of Tox augments effector function, decreases the expression of PD-1, and significantly enhances immunopathology. These changes are linked to a failure in fixing the dysfunctional phenotype in the critical Tcf1+ progenitor population and to impaired epigenetic programing. Surprisingly, the gains in effector function co-incide with declining numbers of Tcf1+ cells and result ultimately in reduced total numbers of pathogen-specific T-cells. Thus, we establish Tox as a critical factor for the development of T-cell dysfunction and establish a clear link between CD8 T-cell intrinsic suppression of effector function and protection against immune-pathology. The terms acute and chronic samples refer to P14 T-cells that were initially activated in acute LCMV (Armstrong) or chronic LCMV (clone-13) infections. 4 weeks later, the P14 T cells were collected, transferred into naive mice, and both then re-expanded in acute LCMV (Armstrong) infection. 8 days later P14 T-cells were collected and analysed.

2019-07-03 | GSE132027 | GEO

Expression Data from Memory P14 Tg CD8 T cells after either saline mock-infection, Pichinde Virus Infection (bystander infection) or Pichinde Virus infection with daily treatment with anti-CD122 (clone TM-b1)

Project description:Exposure to inflammatory cytokines driven by bystander cytokines can have profound effects on the function of memory CD8 T cells. Here we transferred a 1-5X10^4 of P14 TCR-tg T cells (specific for gp33-41 of LCMV) on day -1 followed by infection with 2X10^5 PFU of LCMV Armstrong ip to generate memory P14 populations. Mice were rested for >50 days before further challenge. Mice containing memory P14 populations were either mock-infected with saline, infected with 2X10^6 Pichinde Virus ip (no cross-reactivity wtih LCMV gp33-41) or infected with 2X10^6 Pichinde Virus ip together with daily injections of 200 micrograms of anti-CD122 antibody (clone TM-b1). On day 4 following indicated treatments P14s were flow sorted and RNA was extracted from 1X10^6 cells using an RNeasy kit (Qiagen). Each group had 3 biological replicates. Transcriptomes were compared by DAVID analysis (p<0.01, Fold-Change > 1.5) 3 biological replicates per group. Groups included P14 from mock-infected mice, P14 from Pichinde virus infected mice and P14 from Pichinde virus and anti-cd122 treated mice.

2015-09-01 | E-GEOD-69791 | biostudies-arrayexpress

Gene expression profile analysis of mouse whole spleen following infection by lymphocytic choriomeningitis virus (LCMV), comparing LCMV-Armstrong and LCMV-Clone 13 expression patterns at 0, 5, 9, and 30 days

Project description:To identify mechanisms behind immunosuppression during virus infections, we infected mice with LCMV-Armstrong and LCMV-Clone 13 expression patterns. LCMV-Armstrong induces a T-cell reaction that resolves infection within 8-10 days, while LCMV-Clone13 generates a persisten infection through immunosuppression. We used microarray to uncover splenic gene expression patterns specific to each LCMV infection at 5, 9, and 30 days C57BL6 mice, 6-10 weeks old, were infected with LCMV-Armstrong and LCMV-Clone 13 or left uninfected (naïve). At days 5, 9, and 30 whole spleens were harvested for RNA extraction and hybridization on Affymetric microarray.

2013-02-15 | E-GEOD-44322 | biostudies-arrayexpress

Novel lymphocytic choriomeningitis virus strain sustains abundant exhausted progenitor CD8 T cells without systemic viremia

Project description:Lymphocytic choriomeningitis virus (LCMV) is the prototypic arenavirus and a natural mouse pathogen. LCMV Armstrong, an acutely resolved strain, and LCMV Clone 13, a mutant that establishes chronic infection, have provided contrasting infection models that continue to inform the fundamental biology of T cell differentiation, regulation of exhaustion, and response to checkpoint blockade. Here, we report the isolation and characterization of LCMV Minnesota (LCMV-MN), which was naturally transmitted to laboratory mice upon cohousing with pet shop mice and shares 80-95% amino acid homology with previously characterized LCMV strains. Infection of laboratory mice with purified LCMV-MN resulted in viral persistence that was intermediate between LCMV Armstrong and Clone 13, with widely disseminated viral replication and viremia that was controlled within 15-30 days, unless CD4 T cells were depleted prior to infection. LCMV-MN responding CD8+ T cells biased differentiation towards the recently described PD1+ CXCR5+ Tim-3lo stem-like CD8+ T cell population (also referred to as T exhausted progenitors, Tpex) that effectuates responses to PD-1 blockade checkpoint inhibition, a therapy that rejuvenates responses against chronic infections and cancer. This subset resembled previously characterized PD1+ TCF1+ stem-like CD8+ T cells by transcriptional, phenotypic, and functional assays, yet was atypically abundant. LCMV-MN may provide a tool to better understand the breadth of immune responses in different settings of chronic antigen stimulation as well as the ontogeny of T exhausted progenitors and the regulation of responsiveness to PD-1 blockade.

2022-08-22 | GSE207983 | GEO

Memory-like CD8 T-cells sustain the immune response to chronic viral infections.

Project description:We have discovered a small subpopulation of virus-specific CD8 T-cells that sustains the T-cell response in chronic infections. These cells are defined by - and depend on - the expression of the transcription factor Tcf1 (T cell factor 1) and show key characteristics of central memory cells while lacking an effector signature. Unlike conventional memory cells, Tcf1+ T-cells display hallmarks of an âexhaustedâ phenotype, including the expression of certain inhibitory receptors. Naive Tcf1-GFP+ P14 cells (Naive) were transferred into Vb5 recipient mice (CD45.1) prior to infection with LCMV clone 13 (c13). Tcf1-GFP+ P14 cells (chronic Tcf1+) and Tcf1-GFP- P14 cells (chronic Tcf1-) were flow sorted on day 28 post infection. Naive Tcf1-GFP+ P14 cells (Naive) were also transferred into C57BL/6 hosts (CD45.1.2) prior to infection with LCMV Armstrong (Arm). Tcf1-GFP+ P14 cells (memory Tcf1+) and Tcf1-GFP- P14 cells (memory Tcf1-) were flow sorted on day 28 post infection. Total RNA was extracted, cDNA libraries prepared and sequencing was performed using Illumina HiSeq 2500 technology.

2016-08-22 | E-GEOD-83978 | biostudies-arrayexpress

2013-02-15 | GSE44322 | 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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