Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell analysis of CX3CR1+ cells reveal a pathogenic role for BIRC5+ myeloid proliferating cells driven by Staphylococcus aureus leukotoxins

ABSTRACT: Our previous studies identified a population of stem cell-like proliferating myeloid cells within inflamed tissues that could serve as a reservoir for tissue macrophages to adopt different activation states depending on the microenvironment. By lineage tracing cells derived from CX3CR1+ precursors in mice during infection and profiling by scRNA-seq, here we identify a cluster of BIRC5+ myeloid cells that expanded in the liver during either chronic infection with the parasite Schistosoma mansoni or the bacterial pathogen Staphylococcus aureus. In the absence of tissue damaging toxins, S. aureus infection does not elicit these BIRC5+ cells. Moreover, deletion of BIRC5 from CX3CR1 expressing cells results in improved survival during S. aureus infection. Hence, the combination of scRNA-Seq and genetic fate mapping CX3CR1+ cells revealed a toxin dependent pathogenic role for BIRC5 in myeloid cells during S. aureus infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE232996 | GEO | 2023/06/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A role for BCL6 in maintaining CX3CR1+ CD4+ T cells during helminth infection

Project description:Distinct subsets of T lymphocytes express CX3CR1 under inflammatory conditions, but little is known about CX3CR1+ CD4+ T cells during Type 2 inflammation in helminth infections. Here, we used a fate-mapping mouse model to characterize CX3CR1+ CD4+ T cells during both acute Nippostrongylus brasiliensis and chronic Schistosoma mansoni helminth infections, revealing CX3CR1+ CD4+ T cells to be an activated tissue homing subset with varying capacity for cytokine production. Tracking these cells over time revealed that maintenance of CX3CR1 itself along with a TH2 phenotype conferred a survival advantage in the inflamed tissue. Single-cell RNA-sequencing analysis of fate-mapped CX3CR1+ CD4+ T cells from both the peripheral tissue and the spleen revealed a considerable level of diversity and identified a distinct population of BCL6+ TCF-1+ PD1+ CD4+ T cells in the spleen during helminth infections. Conditional deletion of BCL6 in CX3CR1+ cells result in fewer CX3CR1+ CD4+ during infection, indicating a role in sustaining CD4+ T cell responses to helminth infections. Overall, our studies revealed the behavior and heterogeneity of CX3CR1+ CD4+ T cells during Type 2 inflammation in helminth infections and identified BCL6 to be important in their maintenance

2023-08-12 | GSE239846 | GEO

RNA sequencing comparison of CXCR3+ and CX3CR1+ CD4+ epitope specific T cells from Se-infected mice.

Project description:Interferon-γ (IFN-γ)-producing CD4+ T helper-1 (Th1) cells are critical for protection from microbes that infect the phagosomes of myeloid cells. We assessed Th1 cell generation in vivo by studying antigen-specific CD4+ T cells during infection with the phagosomal pathogen Salmonella enterica. We found that this infection induced two varieties of Th1 cells, one expressing CXCR3 and one expressing CX3CR1. We performed RNA sequencing on these two types of Th1 cells that were specific for the LpdAp:I-Ab epitope from B6 x 129 F1 mice 30 days after Salmonella enterica infection to gain information about the differences between these types of Th1 cells and how those differences might relate to protective immunity. We report results for CXCR3+ CX3CR1- and CXCR3- CX3CR1+ LpdAp:I-Ab-tetramer binding cells.

2021-03-18 | GSE168300 | GEO

CX3CR1/Fractalkine receptor expression separates memory CD8+ T cells with distinct functional profiles (expression)

Project description:Memory T cells are important for protective immunity against infectious microorganisms. Such protection is achieved by cooperative action of memory T cell populations that differ in their tissue localization and functionality. We report on the identification of the fractalkine receptor CX3CR1 as marker for stratification of memory T cells with cytotoxic effector function from those with proliferative function in both, mice and man. Based on CX3CR1 and CD62L expression levels four distinct memory T cell populations can be distinguished based on their functional properties. Transcriptome and proteome profiling revealed that CX3CR1 expression was superior to CD62L to resolve memory T cell functionality and allowed determination of a core signature of memory T cells with cytotoxic effector function. This identifies a CD62Lhi CX3CR1+ memory T cell population with an identical gene signature to CD62LlowCX3CR1+ effector memory T cells. In lymph nodes, this so far unrecognized CD62LhiCX3CR1+ T cell population shows a distinct migration pattern and anatomic positioning compared to CD62LhiCX3CR1neg TCM. Furthermore, CX3CR1+ memory T cells were scarce or absent during chronic HBV, HCV and HIV infection in man and chronic LCMV infection in mice confirming the value of CX3CR1+ in understanding principles of protective immune memory. CD8+ T cells were isolated and directly assessed or incubated with DC or LSEC. After harvesting, cells were immediately lysed in Trizol (Invitrogen) before storage at -80Â°C for RNA isolation.

2016-06-10 | E-GEOD-63118 | biostudies-arrayexpress

CX3CR1/Fractalkine receptor expression separates memory CD8+ T cells with distinct functional profiles (RNA-seq)

Project description:Memory T cells are important for protective immunity against infectious microorganisms. Such protection is achieved by cooperative action of memory T cell populations that differ in their tissue localization and functionality. We report on the identification of the fractalkine receptor CX3CR1 as marker for stratification of memory T cells with cytotoxic effector function from those with proliferative function in both, mice and man. Based on CX3CR1 and CD62L expression levels four distinct memory T cell populations can be distinguished based on their functional properties. Transcriptome and proteome profiling revealed that CX3CR1 expression was superior to CD62L to resolve memory T cell functionality and allowed determination of a core signature of memory T cells with cytotoxic effector function. This identifies a CD62Lhi CX3CR1+ memory T cell population with an identical gene signature to CD62LlowCX3CR1+ effector memory T cells. In lymph nodes, this so far unrecognized CD62LhiCX3CR1+ T cell population shows a distinct migration pattern and anatomic positioning compared to CD62LhiCX3CR1neg TCM. Furthermore, CX3CR1+ memory T cells were scarce or absent during chronic HBV, HCV and HIV infection in man and chronic LCMV infection in mice confirming the value of CX3CR1+ in understanding principles of protective immune memory. CD8+ T cells were isolated and directly assessed. After harvesting, cells were immediately lysed in Trizol (Invitrogen) before storage at -80Â°C for RNA isolation.

2016-06-10 | E-GEOD-63144 | biostudies-arrayexpress

Chromatin accessibility landscapes of CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

Project description:During chronic viral infection, pathogen-specifc CD8+ T cells develop into three main phenotypically and functionally distinct subsets: TCF1hi progenitor, PD-1hi exhausted, and recently identied CX3CR1+ cytotoxic effector cells. Although genetic programs governing progenitor and exhausted subset formation have been well-studied, how CX3CR1+ effector CD8+ T cell differentiation is transcriptionally and epigentically regulated remains elusive. In this study, our single cell transcriptomics and epigenetic assays revealed that three subsets of virus-specific cells were governed by distinct gene regulatory networks (GRNs) and epigenetic landscapes. Computational analyses demonstrated a striking similarity between the CX3CR1+ subset and short-live effector cells (SLECs) from acute LCMV infection. Consistently, genetic deletion of T-bet (Tbx21) significantly diminished the formation and function of the CX3CR1+ subset. Importantly, we identify that the transcription factor (TF) BATF is required to maintain a permissive chromatin structure that allows differentiation transition from TCF1+ progenitor to CX3CR1+ effector cells. Intriguingly, haplodificiency of BATF in CD8+ T cells abolished CX3CR1+ effector subset formation. Lastly, we found that BATF directly bound to key genetic regions such as Tbx21 and modulated their enhancer accessibility to facilitate progenitor to CX3CR1+ effector cell transition. These mechanistic insights can be harnessed to overcome T cell exhaustion in treating chronic infections and cancer.

2021-05-22 | GSE149752 | GEO

Genome-wide maps of histone modifications in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

2021-05-22 | GSE149810 | GEO

CUT&Tag ChIP-seq analysis of BATF in CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

2021-06-02 | GSE149796 | GEO

CX3CR1/Fractalkine receptor expression separates memory CD8+ T cells with distinct functional profiles (expression)

2016-06-10 | GSE63118 | GEO

CX3CR1/Fractalkine receptor expression separates memory CD8+ T cells with distinct functional profiles (RNA-seq)

2016-06-10 | GSE63144 | GEO

Chromatin accessibility landscapes of CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

Project description:Chromatin accessibility landscapes of CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

| PRJNA630086 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data