Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of ACKR3+ and ACKR3- Marginal Zone B cells (MZBs) in mice

ABSTRACT: The marginal zone (MZ) of the spleen contains a specialized set of innate-like B cells that are in direct contact with the blood. Here we show that expression of the atypical chemokine receptor 3 (ACKR3) defines two phenotypically, transcriptionally and functionally distinct, equal-sized populations of mouse MZ B cells (MZBs). The ACKR3-expressing population is required for optimal development and function of the MZ and for the differentiation and positioning of all MZBs. In the absence of ACKR3 expression on B cells the MZ is distorted and the MZBs fail to deliver blood-borne antigens to follicular dendritic cells (FDCs), leading to a reduced early humoral immune response. Effective reconstitution of MZ deficient CD19ko mice with either of the two MZB subsets shows that ACKR3- MZBs can differentiate into the more mature ACKR3+ MZBs, but not vice versa. The phenotype of CD19ko mice lacking a MZ is readily rescued by the adoptive transfer of ACKR3-sufficient, and to a much lower degree by ACKR3-deficient follicular B cells (FoBs), indicating that ACKR3 expression is crucial for the establishment of the MZ developmental niche. Similarly, the inability of CD19ko mice to respond to T-independent antigen is rescued when ACKR3-proficient, but not ACKR3-deficient FoBs are adoptively transferred. Accordingly, ACKR3-deficient FoBs are able to reconstitute the MZ if the niche is pre-established by ACKR3 proficient MZBs. Our data uncover a new unexpected role of ACKR3 on B cells for forming the splenic microarchitecture.

ORGANISM(S): Mus musculus

PROVIDER: GSE126860 | GEO | 2020/06/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Access to follicular dendritic cells is a pivotal step in murine chronic lymphocytic leukemia B cell activation and proliferation

Project description:In human chronic lymphocytic leukemia (CLL) pathogenesis B cell antigen receptor signaling seems important for leukemia B cell ontogeny, whereas the microenvironment influences B cell activation, tumor cell lodging and provision of antigenic stimuli. Using the murine E?-Tcl1 CLL model, we demonstrate that CXCR5-controlled access to follicular dendritic cells (FDCs) confers proliferative stimuli to leukemia B cells. Intravital imaging revealed a marginal zone B cell-like leukemia cell trafficking route. Murine and human CLL cells reciprocally stimulated resident mesenchymal stromal cells through lymphotoxin-?-receptor activation, resulting in CXCL13 secretion and stromal compartment remodeling. Inhibition of lymphotoxin/lymphotoxin-?-receptor signaling or of CXCR5 signaling retards leukemia progression. Thus, CXCR5 activity links tumor cell homing, shaping a survival niche, and access to localized proliferation stimuli. This GEO dataset is comprised of GEP measurements for EµTCL mouse CD5+CD19+ tumor cells and healthy WT controls, including healthy MZB cells and B1 cells. 6 measurements are for WT EµTCL1 mice, 5 for the CXCR5-KO EµTCL1 genotype. MZB and B1 cells were pooled from 15 animals. WT reference was obtained from 5 WT animals

2014-09-01 | E-GEOD-60925 | biostudies-arrayexpress

Glutathione-dependent redox balance characterizes the distinct metabolic properties of follicular and marginal zone B cells

Project description:The metabolic principles underlying the differences between follicular and marginal zone B cells (FoB and MZB, respectively) are not well understood. Here we show, by studying mice with B cell-specific ablation of the catalytic subunit of glutamate cysteine ligase (Gclc), that glutathione synthesis affects homeostasis and differentiation of MZB to a larger extent than FoB, while glutathione-dependent redox control contributes to the metabolic dependencies of FoB. Specifically, Gclc ablation in FoB induces metabolic features of wild-type MZB such as increased ATP levels, glucose metabolism, mTOR activation and protein synthesis. Furthermore, Gclc-deficient FoB have a block in the mitochondrial electron transport chain (ETC) due to diminished complex I and II activity and thereby accumulate the tricarboxylic acid cycle metabolite succinate. Finally, Gclc deficiency hampers FoB activation and antibody responses in vitro and in vivo, and induces susceptibility to viral infections. In summary, Gclc is required to ensure the development of MZB, the integrity of the mitochondrial ETC in FoB and it is crucial for antibody-mediated immunity.

2022-01-25 | GSE194419 | GEO

Marginal zone B cells control follicular helper T cell response to high cholesterol diet

Project description:Splenic innate-like marginal zone B (MZB) cells are strategically positioned at the interface between the circulating blood and lymphoid tissue, where they initiate rapid immune responses to blood-borne antigens. Here, we find that selective genetic deletion of MZB cells substantially increases the follicular helper T (Tfh) cell and germinal center (GC) response to high cholesterol diet (HCD), which leads to T cell-dependent acceleration of atherosclerosis. We show that MZB cells activate a homeostatic program in response to HCD, in which upregulation of the transcription factor Atf3 plays a determinant regulatory role. Shuttling of MZB cells to the follicle is dispensable for their regulatory properties on Tfh cells. Instead, HCD promotes increased interaction between MZB and (pre-)Tfh cells outside the follicle, and upregulates MZB cell expression of Cd274 in an Atf3-dependent manner. Interaction between MZB and Tfh cells leads to Cd274-mediated suppression of Tfh cell motility, limits Tfh cell accumulation in the follicle and suppresses the pro-atherogenic Tfh/GC response. Our findings reveal a previously unsuspected role for MZB cells in the control of Tfh/GC response to a cholesterol diet, and uncover a new mechanism through which MZB cells can couple their unique metabolic and innate immune properties and use them to maintain a tolerogenic state. The results may have broad (patho)physiological implications.

2016-12-01 | GSE71699 | GEO

Programming of marginal zone B cell fate by basic krüppel-like factor (BKLF/KLF3)

Project description:Gene expression analysis of splenic follicular B cells and marginal zone B cells from B6 and CD19:KLF3 transgenic mice Comparing KLF3-transgenic and non-transgenic follicular B cells by RNA-microarray revealed that KLF3 regulates a subset of genes that was similarly up-/downregulated upon normal MZ B cell differentiation. Indeed, KLF3 expression overcame the lack of MZ B cells caused by different genetic alterations, such as CD19-deficiency or blockade of B-cell activating factor (BAFF)-receptor signaling, indicating that KLF3 may complement alternative NF-κB signaling. Thus, KLF3 is a driving force towards MZ B cell maturation. RNA of splenic follicular B cells and marginal zone B cells were obtained from 4 different mice per group (B6 and CD19:KLF3 mice). 16 samples = 8 individual mice x 2 B cell subsets.

2011-01-29 | E-GEOD-26948 | biostudies-arrayexpress

Transcriptome profiling of H3K27me3 demethylase deficient B cells

Project description:To assess how H3K27me3 demethylases, UTX and JMJD3, regulate B cell and plasma cell trasncriptomes. RNA-seq was performed on the following populations from control (CreCtrl) and double knockout (dKO) mice: 1) naïve marginal zone B (MZB) cells and follicular B (FOB) cells from control (CreCtrl) and double knockout (dKO) mice, 2) PC generated after three days of ex vivo culture of MZB or FOB cells, 3) PC generated at three days post in vivo stimulation with LPS

2022-02-01 | GSE185095 | GEO

Transcription profiling of mouse follicular and marginal zone B-cells

Project description:Immature B cells in spleens of mouse and human differentiate into at least two subsets of mature B cells, the follicular (FO) B cells and the marginal zone (MZ) B cells, but functions, maturation and other properties of these cells are largely unknown. To solve these questions, in this study, we performed transcriptome analyses of FO and MZ B cells sorted from spleens of normal unimmunized mice using gene chips. By comparison of gene expression profiles between FO and MZ B cells, we identified 1226 genes that are expressed higher in FO B cells than in MZ B cells. On the other hand, 1734 genes were found to be expressed higher in MZ B cells than in FO B cells. We noticed that some of differentially expressed genes have been reportedly characterized in FO and MZ B cells, suggesting the reliability of the analysis. By using FACS analyses, we confirmed that CD36, CD68, and CD49e are expressed on MZ B-cells but not on FO B-cells. These results revealed new phenotypic and functional properties of FO and MZ B cells, and set a molecular basis for further studying differentiation and functions of these mature B cells. Experiment Overall Design: one follicular B cells replicate and one marginal zone B cells replicate were analyzed.

2008-06-12 | E-GEOD-3599 | biostudies-arrayexpress

Programming of marginal zone B cell fate by basic krüppel-like factor (BKLF/KLF3)

2011-01-29 | GSE26948 | GEO

Comparison of gene expression profiles between mouse follicular and marginal zone B-cells

Project description:Immature B cells in spleens of mouse and human differentiate into at least two subsets of mature B cells, the follicular (FO) B cells and the marginal zone (MZ) B cells, but functions, maturation and other properties of these cells are largely unknown. To solve these questions, in this study, we performed transcriptome analyses of FO and MZ B cells sorted from spleens of normal unimmunized mice using gene chips. By comparison of gene expression profiles between FO and MZ B cells, we identified 1226 genes that are expressed higher in FO B cells than in MZ B cells. On the other hand, 1734 genes were found to be expressed higher in MZ B cells than in FO B cells. We noticed that some of differentially expressed genes have been reportedly characterized in FO and MZ B cells, suggesting the reliability of the analysis. By using FACS analyses, we confirmed that CD36, CD68, and CD49e are expressed on MZ B-cells but not on FO B-cells. These results revealed new phenotypic and functional properties of FO and MZ B cells, and set a molecular basis for further studying differentiation and functions of these mature B cells. Keywords: Comparison of gene expression profiles between mouse follicular and marginal zone B-cells

2006-04-21 | GSE3599 | GEO

Gut IgA Enhances Systemic IgG Responses to Pneumococcal Vaccines Through the Commensal Microbiota

Project description:We set up to characterize the global transcriptome of splenic follicular (FO) B cells from control wild type (Wt) and Igha-deficient (IgAKO) mice with the aim of gaining new insights into how translocated gut antigens may impair IgG production to vaccines in the absence of IgA. Splenic Marginal zone (MZ) B cells were also included in this study, as IgA deficiency impaired IgG responses to T-independent immunogens as well.

2024-01-01 | GSE173361 | GEO

Gene expression profiling of spleen marginal zone B cells and spleen follicular B cells in IRF8 conditional KO mice

Project description:Conditional IRF8 KO mice (mice with a conditional allele of Irf8 crossed with CD19-Cre mice) showed increased numbers of both Gene expression data spleen marginal zone (MZ) and Gene expression data spleen follicular (FO) B cells compared to control mice. To evaluate gene expression patterns that distinguished FO or MZ B cells derived from conditional KO and control mice, we used Affymetrix GeneChip® Mouse gene 1.0 ST Array. FACS-sorted MZ and FO B cells from individual mouse were used for RNA extraction and Affyarray hybridization. There were six independent biological replications in each group - six cases of MZ B cells and FO cells in IRF8 conditional KO mice and six cases of MZ B cells and FO cells in control WT mice.

2010-12-20 | E-GEOD-24972 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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