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Paired scRNA-seq and scTCR-seq of GP33-specific CD8 T cells in chronic LCMV infection

ABSTRACT: Paired scRNA-seq and scTCR-seq of GP33-specific CD8 T cells in chronic LCMV infection

PROVIDER: PRJNA849772 | ENA |

REPOSITORIES: ENA

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Paired scRNA-seq and scTCR-seq of GP33-specific CD8 T cells in chronic LCMV infection

Project description:Chronic viral infection results in CD8 T cell exhaustion. Here, we use paired single-cell RNA sequencing (scRNA-seq) and single-cell T cell receptor sequencing (scTCR-seq) to investigate CD8 T cell phenotypic and clonal heterogeneity in multiple mice during the late stage of LCMV Clone 13 infection.

2022-10-23 | GSE206230 | GEO

RNA-seq of LCMV GP33-specific CD8 TCR transgenic cells (P14) primed at the onset versus in the midst of persistent LCMV-Clone 13 viral infection

Project description:Altered CD8 T cell differentiation and functional exhaustion prevent control of chronic virus infection and cancer. Yet, how fate commitment and exhaustion are determined and dynamically modulated throughout persistent infection are unclear. We compared the activation and differentiation of LCMV GP33-specific CD8 TCR transgenic cells (P14) primed at the onset versus in the midst of established persistent LCMV-Clone 13 viral infection. LCMV GP33-specific CD8 TCR transgenic (P14) cells were injected into naïve mice immediately infected with LCMV-Cl13 (Early priming) or into mice that had been infected 21 days earlier with LCMV-Cl13 (Late Priming). Sixty hours post-priming P14 cells were sorted from mice and subjected to RNA seq. We show early primed cells very rapidly exhibit a transcriptional profile of robust activation, effector differentiation and dysfunction, while late primed cells have increased expression of genes involved in memory differentiation and maintenance.

2018-10-09 | GSE105044 | GEO

Identification of GP33-specific CD8 T cell clones responding to chronic infection with LCMV-Clone13

Project description:T cells specific for a certain antigen are a heterogeneous population characterized by cells expressing different T Cell Receptors (TCRs). As the TCR determines the avidity of a T cell clone for its cognate antigen, this feature has also a significant impact on the fate of such clone during antigenic challenge. In the context of chronic viral infection, T cells specific for the chronic virus differentiate into exhausted cells with limited functionality. We find that, in the process of exhaustion following infection with LCMV-Clone13, certain clones of CD8 T cells specific for the LCMV immunodominant epitope GP33 are enriched compared to others.

2022-10-23 | GSE210116 | GEO

RNA-Seq of CD8+ T cell subsets during LCMV infection [RNA-seq_D8_Brd4_KO]

Project description:Brd4 deficient and WT GP33-tetramer+ cells were sorted from spleens on D8 of LCMV infection. Tamoxifen was administered on days 5-7 of infection to induce to deletion of Brd4. KLRG1hiCD127lo TE, KLRG1loCD127lo EEC, and KLRG1loCD127hi MP cells were sorted for RNAseq analysis.

2021-05-21 | GSE173512 | GEO

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

Longitudinal expression data from CD8+ T cells responding to LCMV-Armstrong or LCMV-Clone 13

Project description:During acute viral infections, naïve CD8+ T cells differentiate into effector CD8+ T cells and, after viral control, into memory CD8+ T cells. Memory CD8+ T cells are highly functional, proliferate rapidly upon reinfection and persist long-term without antigen. In contrast, during chronic infections, CD8+ T cells become “exhausted” and have poor effector function, express multiple inhibitory receptors, possess low proliferative capacity, and cannot persist without antigen. To compare the development of functional memory T cells with poorly functional exhausted T cells, we generated longitudinal transcriptional profiles for each. Naive CD44Lo CD8+ T cells were isolated and sorted from uninfected C57BL/6 mice and H2-Db GP33-specific CD8+ T cells were sorted using MHC-I tetramers at d6, 8, 15, and 30 p.i. with either LCMV Arm or LCMV clone 13. RNA from these CD8+ T cells was processed, amplified, labeled, and hybridized to Affymetrix GeneChip MoGene 1.0 st microarrays

2012-11-23 | E-GEOD-41867 | biostudies-arrayexpress

RNA-seq of LCMV GP33-specific CD8 TCR transgenic cells (P14) primed at the onset versus in the midst of persistent LCMV-Clone 13 viral infection

Project description:RNA-seq of LCMV GP33-specific CD8 TCR transgenic cells (P14) primed at the onset versus in the midst of persistent LCMV-Clone 13 viral infection

| PRJNA414459 | ENA

Identification of GP33-specific CD8 T cell clones responding to chronic infection with LCMV-Clone13

Project description:Identification of GP33-specific CD8 T cell clones responding to chronic infection with LCMV-Clone13

| PRJNA863674 | ENA

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

Project description: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.

2023-10-17 | GSE204693 | GEO

The LCMV gp33-specific memory T cell repertoire narrows with age.

Project description:BACKGROUND:The memory response to LCMV in mice persists for months to years with only a small decrease in the number of epitope specific CD8 T cells. This long persistence is associated with resistance to lethal LCMV disease. In contrast to studies focused on the number and surface phenotype of the memory cells, relatively little attention has been paid to the diversity of TCR usage in these cells. CD8+ T cell responses with only a few clones of identical specificity are believed to be relatively ineffective, presumably due to the relative ease of virus escape. Thus, a broad polyclonal response is associated with an effective anti-viral CD8+ T cell response. RESULTS:In this paper we show that the primary CD8+ T cell response to the LCMV gp33-41 epitope is extremely diverse. Over time while the response remains robust in terms of the number of gp33-tetramer+ T cells, the diversity of the response becomes less so. Strikingly, by 26?months after infection the response is dominated by a small number TCR? sequences. In addition, it is of note the gp33 specific CD8+ T cells sorted by high and low tetramer binding populations 15 and 22?months after infection. High and low tetramer binding cells had equivalent diversity and were dominated by a small number of clones regardless of the time tested. A similar restricted distribution was seen in NP396 specific CD8+ T cells 26?months after infection. The identical TCRV? sequences were found in both the tetramerhi and tetramerlo binding populations. Finally, we saw no evidence of public clones in the gp33-specific response. No CDR3 sequences were found in more than one mouse. CONCLUSIONS:These data show that following LCMV infection the CD8+ gp33-specific CD8 T cell response becomes highly restricted with enormous narrowing of the diversity. This narrowing of the repertoire could contribute to the progressively ineffective immune response seen in aging.

| S-EPMC3472190 | biostudies-literature

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