Mus musculus breed:C57BL/6
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA344523 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In response to acute infection, naive CD8+ T cells expand, differentiate into effector cells and then contract to a long-lived pool of memory cells after pathogen clearance. During chronic infections or in tumors, CD8+ T cells acquire an “exhausted” phenotype. Here we present genome-wide comparisons of chromatin accessibility and gene expression from endogenous CD8+ T cells responding to acute and chronic viral infection using ATAC-seq and RNA-seq. Acquisition of effector, memory or exhausted phenotypes was associated with stable changes in chromatin accessibility away from the naive T cell state. Regions differentially accessible between functional subsets in vivo were enriched for binding sites of transcription factors known to regulate these subsets, including E2A, BATF, IRF4, T-bet and TCF1. Exhaustion-specific accessible regions were enriched for consensus binding sites for NFAT and Nr4a family members, indicating that chronic stimulation confers a unique accessibility profile on exhausted cells.
2016-12-13 | GSE88987 | GEO
Project description:Dynamic changes in chromatin accessibility in CD8+ T cells responding to viral infection
| PRJNA349462 | ENA
Project description:The goal of this study was to identify the molecular programming using ATAC-seq of CD8 T cells responding to different viral infections. Mice were infected with either LCMV Armstrong to model an acute infection or LCMV Clone-13 to model a chronic infection. At various time points following infection, virus-specific CD8 T cells were purified and ATAC-seq performed. These data identify the changes in chromatin accessibility associated with acute infections and the establishment of functional memory versus those accessibility changes associated with chronic infection.
2017-01-31 | GSE83081 | GEO
Project description:Compendium of high-throughput sequencing datasets derived from murine CD8+ T cells responding to infection, profiled by RNA-seq, ChIP-seq, and ATAC-seq at Naïve, Effector, and Memory timepoints across the Kaech, Goldrath, and Pereira labs, and ChIP-seq of various transcription factors across several labs Submission contains both original data from the Kaech lab and reanalysis of data from the Pereira and Goldrath labs, as well as various other labs corresponding to individual transcription factor ChIP-seq datasets, totaling to 96 reanalyzed GSM samples across several GSE series Included GSE series are: GSE95237 (Genome-wide maps of chromatin state and chromatin accessibility in CD8 T cell subsets), GSE95238 (Epigenetic landscapes reveal transcription factors that regulate CD8+ T cell differentiation), GSE88987 (Dynamic changes in chromatin accessibility in CD8+ T cells responding to viral infection), GSE58075 (Genome-wide mapping of Myc, AP4, and phosphorylated RNA polymerase II binding in activated CD8 T cells by ChIP sequencing), GSE54191 (ChIP-Seq analysis of BATF, IRF4, the Jun proteins, and histone modifications in effector CD8+ T cells), GSE20898 (Genome-wide Analyses of Transcription Factor GATA3-Mediated Gene Regulation in Distinct T Cell Types), GSE46943 (Transcription Factor Foxo1 Controls Memory CD8+ T Cell Responses To Infection [ChIP-Seq]), GSE72997 (ChIP-Seq analysis of Helios and histone modifications in CD4+ and CD8+ Tregs), GSE50128 (Genome-wide maps of Runx3 bound regions in splenic IL-2-activated CD8+ T cells), GSE72565 (Binding of STAT5 upon IL-2 treatment to genomic sites in mouse CD8 T cells costimulated in vivo through CD134 plus CD137), GSE49930 (The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [ChIP-seq]), and GSE52070 (Genome-wide maps of Tcf1 binding locations in splenic CD8 T cells)
2018-03-17 | GSE111902 | GEO
Project description:Acute viral infection typically generates functional effector CD8+ T cells that aid in pathogen clearance. However, during acute viral lower respiratory infection (LRI), lung CD8+ T cells are functionally impaired and do not optimally control viral replication, while spleen CD8+ T cells specific for the same viral epitopes remain fully functional. To better understand the mechanisms governing lung CD8+ T cell impairment, we used flow cytometry to sort anti-viral CD8+ T cells during viral LRI. Lung and spleen cells were stained with MHC-class I tetramers representing the immunodominant anti-viral CD8+ T cell epitope. We then sorted to high purity: naïve CD8+ T cells, spleen epitope-specific CD8+ T cells, lung epitope-specific CD8+ cells and secondary infection lung epitope-specific CD8+ T cells. We then performed a genome wide transcriptional analysis of these cells to characterize the gene expression profile of lung CD8+ T cell impairment.
2015-10-01 | GSE53349 | GEO
Project description:To gain insights into how PBAF complex regulates dynamic chromatin structure changes in LCMV-specific CD8+ T cells during chronic viral infection and examine the how PBAF-deficiency alters the transcriptional and epigenetic heterogeneity of CD8+ T cells, we performed single cell RNA + ATAC multiomic sequencing on Arid2- and Pbrm1-deficient CD8+ T cells and their wild-type counterpart.
2023-06-22 | GSE222346 | GEO
Project description:Currently there is limited knowledge of changes in genome-wide chromatin accessibility during Mycobacterium tuberculosis (Mtb) infection and whether host phosphatases such as PPM1A play a role in this process. Using combinatorial chromatin accessibility (ATAC-seq) and transcriptomics (RNA-seq) profiling of wild-type (WT), PPM1A knockout (△PPM1A) and PPM1A overexpressing (PPM1A+) macrophages, we demonstrate that Mtb infection induces global chromatin remodeling consistent with changes in gene expression signatures. The strongest concordant chromatin accessibility and gene expression signature triggered by Mtb infection was enriched for genes involved in the type I interferon (IFN) signaling pathways. Modulation of PPM1A expression results in altered chromatin accessibility signatures during Mtb infection that are reflected in the total number, chromosome location and directionality of change.
2023-02-08 | GSE211976 | GEO
Project description:Currently there is limited knowledge of changes in genome-wide chromatin accessibility during Mycobacterium tuberculosis (Mtb) infection and whether host phosphatases such as PPM1A play a role in this process. Using combinatorial chromatin accessibility (ATAC-seq) and transcriptomics (RNA-seq) profiling of wild-type (WT), PPM1A knockout (△PPM1A) and PPM1A overexpressing (PPM1A+) macrophages, we demonstrate that Mtb infection induces global chromatin remodeling consistent with changes in gene expression signatures. The strongest concordant chromatin accessibility and gene expression signature triggered by Mtb infection was enriched for genes involved in the type I interferon (IFN) signaling pathways. Modulation of PPM1A expression results in altered chromatin accessibility signatures during Mtb infection that are reflected in the total number, chromosome location and directionality of change.
2023-02-08 | GSE211974 | GEO
Project description:Changes in chromatin accessibility assocaiated with CD8 T cell responses to viral infections
| PRJNA325011 | ENA
Project description:Some viruses have established an equilibrium with their host. African green monkeys (AGM) display persistent high viral replication in blood and intestine during Simian immunodeficiency virus (SIV) infection but resolve systemic inflammation after acute infection and lack intestinal immune or tissue damage during chronic infection. We show that NKG2 a/c + CD8 + T cells increase in blood and intestine of AGM in response to SIVagm infection in contrast to SIVmac infection in macaques, the latter modeling HIV infection. NKG2 a/c + CD8 + T cells were not expanded in lymph nodes and CXCR5 + NKG2 a/c + CD8 + T cell frequencies further decreased after SIV infection. Genome-wide transcriptome analysis of NKG2 a/c + CD8 + T cells from AGM revealed the expression of NK cell receptors, and of molecules with cytotoxic effector, gut homing, immunoregulatory and gut barrier function, including CD73. NKG2 a/c + CD8 + T cells correlated negatively with IL-23 in the intestine during SIVmac infection. The data suggest a potential regulatory role of NKG2 a/c + CD8 + T cells in intestinal inflammation during SIV/HIV infections.
2021-03-11 | E-MTAB-8664 | biostudies-arrayexpress