Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray analysis of C. rodentium infected colons

ABSTRACT: Defense against attaching and effacing (A/E) bacteria requires the sequential generation of IL-23 and IL-22 to induce protective mucosal responses. While the critical source of IL-22 has been identified as CD4+ and Nkp46+ innate lymphoid cells (ILCs), the precise source of IL-23 is unclear. Here, we use genetic techniques to deplete specific classical dendritic cell (cDC) subsets and analyze immunity to the A/E pathogen Citrobacter rodentium. We find that Zbtb46+ cDCs, and specifically Notch2-dependent intestinal CD11b+ cDCs, but not Batf3-dependent CD103+ cDCs, are required for IL-23 production and immunity against C. rodentium. Notch2 controls cDC differentiation at a terminal step mediated by lymphotoxin signaling. Importantly, these results provide the first demonstration of a non-redundant function of CD11b+ cDCs in vivo. Analysis of genes differentially expressed between WT, Batf3 KO and Notch2 KO colons following C. rodentium infection. Mice were infected with 2 x 10^9 C. rodentium and colons harvested at either Day 4 or Day 9.

ORGANISM(S): Mus musculus

SUBMITTER: Ansuman Satpathy

PROVIDER: E-GEOD-45682 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Microarray analysis of WT and Notch2-deficient classical DC subsets

Project description:Defense against attaching and effacing (A/E) bacteria requires the sequential generation of IL-23 and IL-22 to induce protective mucosal responses. While the critical source of IL-22 has been identified as CD4+ and Nkp46+ innate lymphoid cells (ILCs), the precise source of IL-23 is unclear. Here, we use genetic techniques to deplete specific classical dendritic cell (cDC) subsets and analyze immunity to the A/E pathogen Citrobacter rodentium. We find that Zbtb46+ cDCs, and specifically Notch2-dependent intestinal CD11b+ cDCs, but not Batf3-dependent CD103+ cDCs, are required for IL-23 production and immunity against C. rodentium. Notch2 controls cDC differentiation at a terminal step mediated by lymphotoxin signaling. Importantly, these results provide the first demonstration of a non-redundant function of CD11b+ cDCs in vivo. Analysis of Notch2-dependent genes in CD11b+ and DEC205+ splenic classical DC subsets. Splenocytes were harvested from littermate WT Notch2 f/f C57Bl/6 or Notch2 CD11c-cre C57Bl/6 mice and DC subsets sorted to >95% purity on the FACSAriaII.

2013-06-01 | E-GEOD-45681 | biostudies-arrayexpress

Microarray analysis of WT ESAM+ and ESAM- cDC subsets

Project description:Defense against attaching and effacing (A/E) bacteria requires the sequential generation of IL-23 and IL-22 to induce protective mucosal responses. While the critical source of IL-22 has been identified as CD4+ and Nkp46+ innate lymphoid cells (ILCs), the precise source of IL-23 is unclear. Here, we use genetic techniques to deplete specific classical dendritic cell (cDC) subsets and analyze immunity to the A/E pathogen Citrobacter rodentium. We find that Zbtb46+ cDCs, and specifically Notch2-dependent intestinal CD11b+ cDCs, but not Batf3-dependent CD103+ cDCs, are required for IL-23 production and immunity against C. rodentium. Notch2 controls cDC differentiation at a terminal step mediated by lymphotoxin signaling. Importantly, these results provide the first demonstration of a non-redundant function of CD11b+ cDCs in vivo. Analysis of differentially expressed genes in ESAM+ and ESAM- CD11b+ and DEC205+ splenic classical DC subsets. Splenocytes were harvested from WT C57Bl/6 or WT Cx3cr1-gfp mice and cDC subsets sorted to >95% purity on the FACSAriaII.

2013-06-01 | E-GEOD-45679 | biostudies-arrayexpress

Microarray analysis of WT ESAM+ and ESAM- cDC subsets

2013-06-01 | GSE45679 | GEO

Microarray analysis of C. rodentium infected colons

2013-06-01 | GSE45682 | GEO

Microarray analysis of WT and Notch2-deficient classical DC subsets

2013-06-01 | GSE45681 | GEO

Batf3 maintains Irf8 autoactivation for commitment of a novel clonogenic progenitor of CD8+DCs

Project description:The transcription factors Batf3 and IRF8 are required for development of CD8α+ conventional dendritic cells (cDCs), but the basis for their actions was unclear. Here, we identify two novel Zbtb46+ progenitors that separately generate CD8α+ and CD4+ cDCs and arise directly from the common DC progenitor (CDP). Irf8 expression in the CDP depends on prior PU.1-dependent autoactivation, and specification of pre-CD8 DC progenitors requires IRF8 but not Batf3. However, upon pre-CD8 DC specification, Irf8 autoactivation becomes Batf3-dependent at a CD8α+ cDC-specific enhancer containing multiple AP1-IRF composite elements (AICEs) within the Irf8 superenhancer. CDPs from Batf3-/- mice that specify toward pre-CD8 DCs fail to complete CD8α+ cDC development due to decay of Irf8 autoactivation, and divert to the CD4+ cDC lineage. Examination of histone modifications (H3K27ac and H3K4me1) and 2 transcription factors (Batf3 and Irf8) and the p300 co-factor binding in 3 different dendritic cell subsets

2015-06-08 | E-GEOD-66899 | biostudies-arrayexpress

DOCK8 regulates protective immunity by controlling the function and survival of RORγt+ ILCs

Project description:Retinoic-acid receptor-related orphan receptor-γt-positive (RORγt+) innate lymphoid cells (ILCs) produce interleukin (IL)-22 and IL-17, which are critical for protective immunity against enteric pathogens. The molecular mechanism underlying the development and survival of RORγt+ ILCs is not thoroughly understood. Here we show that Dedicator of cytokinesis 8 (DOCK8), a scaffolding protein involved in cytoskeletal rearrangement and cell migration, is essential for the protective immunity against Citrobacter rodentium. A comparative RNA sequencing-based analysis reveals an impaired induction of antimicrobial peptides in the colon of DOCK8-deficient mice, which correlates with high susceptibility to infection and a very low number of IL-22-producing RORγt+ ILCs in their GI tract. Furthermore, DOCK8-deficient RORγt+ ILCs are less responsive to IL-7 mediated signaling, more prone to apoptosis and produce less IL-22 due to a defect in IL-23-mediated STAT3 phosphorylation. Our studies reveal an unsuspected role of DOCK8 for the function, generation and survival of RORγt+ ILCs. Control and DOCK8 KO mice were infected with 2X109 CFU of Citrobacter rodentium and day 8 post infection mice were sacrificed and their colons were harvested (n=5) . Total RNA was purified from the infected colons with RNeasy mini kit (Qiagen). RNA sequencing was performed (pooled RNA sample from five mice in each group) at Genomic Core Facility Southwestern Medical Center, University of Texas.

2014-06-25 | E-GEOD-58765 | biostudies-arrayexpress

Global gene expression profiling of cardiac dendritic cells subsets

Project description:Innate and adaptive immune cells modulate heart failure pathogenesis during viral myocarditis, yet their identity and functions remain poorly defined. In this study we characterized the phenotype, life-cycle and function of different conventional dendritic cells (cDC) populations in the heart, with focus on the 2 major subsets (CD103+ and CD11b+), which differentially rely on local proliferation and precursor recruitment to maintain tissue residency. Following viral infection of the myocardium, cDCs accumulate in the heart coincident with monocyte infiltration and loss of resident reparative embryonic-derived cardiac macrophages. cDC depletion abrogates antigen-specific CD8+ T cell proliferative expansion, transforming subclinical cardiac injury to overt heart failure. Importantly, these effects are mediated by BATF3-dependent CD103+ cDCs. Collectively, our findings definitively identify resident cardiac cDC subsets, define their origins, and implicate an essential role for CD103+ cDCs in antigen-specific T cell responses during viral myocarditis.

2018-01-01 | GSE102828 | GEO

Batf3 maintains Irf8 autoactivation for commitment of a novel clonogenic progenitor of CD8+DCs

2015-06-08 | GSE66899 | GEO

Single-cell transcriptomic analysis of mouse lung CD11b+ dendritic cells post allergic sensitization

Project description:Conventional dendritic cells (cDCs) in the lung that drive effector T cell differentiation, and initiate allergic responses upon inhalation of allergens. However, since CD11b+ cDCs are heterogeneous, the specific function of each subpopulation has been elusive. To identify subpopulations of CD11b+ cDCs, we performed single cell RNA-sequencing (scRNAS-Seq) of total lung CD11b+ cDCs following inhalation of house dust extracts, and detected multiple clusters based on their differential transcriptomes. The data will be applicable for studies of cDC function in induction of T cell differentiation as well as the maturation pathway of cDCs.

2021-06-25 | GSE156527 | GEO

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