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Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE119943 | GEO | 2019/04/16

REPOSITORIES: GEO

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Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [RNA-seq]

Project description:Stem-like CD8 T cells maintain long-term antiviral CD8 immunity during chronic infection, and share regulatory pathways with memory precursor effector cells generated after acute infection. However, it is unclear whether stem-like CD8 T cells require distinct transcriptional and epigenetic regulation for their longevity and adaptation to the immunosuppressive environment in chronic infection. Here, our comparison of single-cell transcriptomes and epigenetic profiles of CD8 T cells responding to acute and chronic viral infections revealed that stem-like CD8 T cells became distinct from memory precursors before clonal expansion ended. We found that a coexpression gene module containing Tox exhibited higher transcriptional activities and active histone marks in stem-like T cells than memory precursors. Moreover, TOX promoted persistence of antiviral CD8 T cells, and was required for stem-like CD8 differentiation. Our results indicate that stem-like CD8 T cells require unique transcriptional and epigenetic programs for their differentiation and persistence during chronic viral infection.

2019-04-16 | GSE119942 | GEO

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [ChIP-seq]

2019-04-16 | GSE119941 | GEO

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [single-cell RNA-seq]

2019-04-16 | GSE119940 | GEO

Single-cell RNA-seq reveals TOX as a key regulator of CD8<sup>+</sup> T cell persistence in chronic infection.

Project description:Progenitor-like CD8+ T cells mediate long-term immunity to chronic infection and cancer and respond potently to immune checkpoint blockade. These cells share transcriptional regulators with memory precursor cells, including T cell-specific transcription factor 1 (TCF1), but it is unclear whether they adopt distinct programs to adapt to the immunosuppressive environment. By comparing the single-cell transcriptomes and epigenetic profiles of CD8+ T cells responding to acute and chronic viral infections, we found that progenitor-like CD8+ T cells became distinct from memory precursor cells before the peak of the T cell response. We discovered a coexpression gene module containing Tox that exhibited higher transcriptional activity associated with more abundant active histone marks in progenitor-like cells than memory precursor cells. Moreover, thymocyte selection-associated high mobility group box protein TOX (TOX) promoted the persistence of antiviral CD8+ T cells and was required for the programming of progenitor-like CD8+ T cells. Thus, long-term CD8+ T cell immunity to chronic viral infection requires unique transcriptional and epigenetic programs associated with the transcription factor TOX.

| S-EPMC6588409 | biostudies-literature

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection

Project description:Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection

| PRJNA490745 | ENA

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [RNA-seq]

Project description:Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [RNA-seq]

| PRJNA490747 | ENA

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [ChIP-seq]

Project description:Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [ChIP-seq]

| PRJNA490749 | ENA

Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [single-cell RNA-seq]

Project description:Single-Cell Transcriptomics Identifies TOX as a Key Transcriptional Regulator of Progenitor-Like CD8 T Cells in Chronic Infection [single-cell RNA-seq]

| PRJNA490748 | ENA

Single-cell transcriptomics identifies Gadd45b as a regulator of herpesvirus-reactivating neurons

Project description:Single-cell RNA sequencing (scRNA-seq) is a powerful technique for dissecting the complexity of normal and diseased tissues, enabling characterization of cell diversity and heterogeneous phenotypic states in unprecedented detail. However, this technology has been underutilized for exploring the interactions between the host cell and viral pathogens in latently-infected cells. Herein, we use scRNA-seq and single-molecule sensitivity fluorescent in situ hybridization (smFISH) technologies to investigate host single-cell transcriptome changes upon the reactivation of a human neurotropic virus, herpes simplex virus-1 (HSV-1). We identify the stress sensor Growth arrest and DNA damage-inducible 45 beta (Gadd45b) as a critical antiviral host factor that regulates HSV-1 reactivation events in a subpopulation of latently-infected primary neurons. We show that distinct subcellular localization of Gadd45b correlates with the viral late gene expression program, as well as the expression of the viral transcription factor, ICP4. We propose that a hallmark of a "successful" or "aborted" HSV-1 reactivation state in primary neurons is determined by a unique subcellular localization signature of the stress sensor Gadd45b.

| S-SCDT-EMBOR-2021-53543-T | biostudies-other

Transcriptomics identifies STAT3 as a key regulator of hippocampal gene expression and anhedonia during withdrawal from chronic alcohol exposure.

Project description:Alcohol use disorder (AUD) is highly comorbid with depression. Withdrawal from chronic alcohol drinking results in depression and understanding brain molecular mechanisms that drive withdrawal-related depression is important for finding new drug targets to treat these comorbid conditions. Here, we performed RNA sequencing of the rat hippocampus during withdrawal from chronic alcohol drinking to discover key signaling pathways involved in alcohol withdrawal-related depressive-like behavior. Data were analyzed by weighted gene co-expression network analysis to identify several modules of co-expressed genes that could have a common underlying regulatory mechanism. One of the hub, or highly interconnected, genes in module 1 that increased during alcohol withdrawal was the transcription factor, signal transducer and activator of transcription 3 (Stat3), a known regulator of immune gene expression. Total and phosphorylated (p)STAT3 protein levels were also increased in the hippocampus during withdrawal after chronic alcohol exposure. Further, pSTAT3 binding was enriched at the module 1 genes Gfap, Tnfrsf1a, and Socs3 during alcohol withdrawal. Notably, pSTAT3 and its target genes were elevated in the postmortem hippocampus of human subjects with AUD when compared with control subjects. To determine the behavioral relevance of STAT3 activation during alcohol withdrawal, we treated rats with the STAT3 inhibitor stattic and tested for sucrose preference as a measure of anhedonia. STAT3 inhibition alleviated alcohol withdrawal-induced anhedonia. These results demonstrate activation of STAT3 signaling in the hippocampus during alcohol withdrawal in rats and in human AUD subjects, and suggest that STAT3 could be a therapeutic target for reducing comorbid AUD and depression.

| S-EPMC8170676 | biostudies-literature

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