Gene expression analysis of FO B and ABCs of young and aged mice.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE237540 | GEO | 2023/09/14
REPOSITORIES: GEO
Similar Datasets
Project description:The origin and nature of recently discovered age-associated B cells (ABCs) is under investigation. We used a microarray to examine the transcriptional signatures of ABCs, follicular B cells from aged mice (AFO), and follicular B cells from young mice (YFO).
2016-05-20 | GSE81650 | GEO
Project description:Specific metabolic program is required for generation of immune cells and their proper function. Since the description of age-associated or autoimmune-associated B cells (ABCs), there has been a growing interest in the role of these cells in autoimmunity. ABCs have many distinct functional properties, including antigen presentation to T cells and autoantibody production in lupus mouse models. Metabolic properties which support these functions are unknown in ABCs. In this study, we showed that ABCs are metabolically hyperactivated than follicular (FO) B cells. There was an increased glycolysis and oxidative phosphorylation (OXPHOS) in ABCs. In line with this observation, ABCs express key costimulatory molecules for T cell activation with distinct group of cytokines. T cell proliferation and activation were induced by both FO B and ABCs in antigen-dependent manner. However, ABCs induce stronger T cell receptor signaling from naïve CD4+ T cells, leading to differentiation of follicular helper T (Tfh) cells. ABCs actively internalize OVA protein and increased autophagy formation. Treatment of ABCs with metformin suppressed antigen presentation by decreasing antigen uptake, leading to a defective generation of Tfh cells. Taken together, these findings reveal distinct metabolic activity in ABCs and define fundamental connection between metabolism and function within ABCs.
2023-09-06 | GSE214185 | GEO
Project description:Upon immunization with a T cell dependent antigen naive follicular B cells (Fo) are activated and a germinal center reaction is induced. Within the next 2 weeks large germinal centers develop where the process of affinity maturation takes place. To analyze the gene expression profile of resting and activated B cells, follicular B cells (Fo), B cells from early (GC1) and late germinal centers (GC2) were isolated and their gene expression profile compared.
2011-03-29 | GSE28237 | GEO
Project description:Upon immunization with a T cell dependent antigen naive follicular B cells (Fo) are activated and a germinal center reaction is induced. Within the next 2 weeks large germinal centers develop where the process of affinity maturation takes place. To analyze the gene expression profile of resting and activated B cells, follicular B cells (Fo), B cells from early (GC1) and late germinal centers (GC2) were isolated and their gene expression profile compared. Gene expression profiles of Fo versus GC1 and GC2 B cells, respectively. Naïve Fo B cells were isolated from non-immunized BALB/c mice. Germinal center B cells sorted from spleen cell suspensions of BALB/-c mice immunized with the T cell dependent antigen 2-phenyl Oxazolone. GC1 B cells were isolated 7 days after primary immunization. GC2 cells were isolated 15 days after primary immunization. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 µg cRNA hybridized in duplicates for each of the three groups to the GeneChip arrays. Group1: Fo, Group2: GC1, Group3: GC2. Lists of differentially regulated genes were created using High Performance Chip Data Analysis (HPCDA) with Bioretis database (http://www.bioretis-analysis.de). Worldwide data sharing is possible via Bioretis, please ask the authors.
2011-03-29 | E-GEOD-28237 | biostudies-arrayexpress
Project description:Age-associated B cells (ABCs) accumulate in systemic autoimmunity, and contributes to pathogenesis. ABCs are characterized by high expression of CD11c and T-bet. As a transcription factor, T-bet cannot be labeled in live cells with antibodies, so we constructed a reporter mouse strain in which fluorescent protein tdTomato fused to T-bet. Then we sorted ABCs (CD11c+T-bet+CD21- B cell) and non-ABCs (CD11c-T- bet- B cell) from the Bm12-induced lupus model for RNA sequencing.
2023-02-16 | E-MTAB-12568 | biostudies-arrayexpress
Project description:CD11c+ atypical B cells (ABCs) are an alternative memory B cell lineage associated with immunization, infection, and autoimmunity. However, the factors that drive the transcriptional program of ABCs have not been identified, and the function of this population remains incompletely understood. Here we identified candidate transcription factors associated with the ABC population based on a human tonsillar B cell single cell dataset. We identified CD11c+ B cells in mice with a similar transcriptomic signature to human ABCs, and using an optimized CRISPR-Cas9 knockdown screen, we observed that loss of zinc finger E-box binding homeobox 2 (Zeb2) impaired ABC formation. Furthermore, ZEB2 haplo-insufficient Mowat Wilson syndrome (MWS) patients have decreased circulating ABCs in the blood. In Cd23Cre/+Zeb2fl/fl mice with impaired ABC formation, ABCs were dispensable for efficient humoral responses after Plasmodium sporozoite immunization but were required to control recrudescent blood-stage malaria. Immune phenotyping revealed that ABCs drive optimal T follicular helper (Tfh) cell formation and germinal center (GC) responses and they reside at the red/white pulp border likely permitting better access to pathogen antigens for presentation. Collectively, our study shows that ABC formation is dependent upon Zeb2, and these cells can limit recrudescent infection by sustaining GC reactions.
2024-02-09 | GSE213194 | GEO
Project description:CD11c+ atypical B cells (ABCs) are an alternative memory B cell lineage associated with immunization, infection, and autoimmunity. However, the factors that drive the transcriptional program of ABCs have not been identified, and the function of this population remains incompletely understood. Here we identified candidate transcription factors associated with the ABC population based on a human tonsillar B cell single cell dataset. We identified CD11c+ B cells in mice with a similar transcriptomic signature to human ABCs, and using an optimized CRISPR-Cas9 knockdown screen, we observed that loss of zinc finger E-box binding homeobox 2 (Zeb2) impaired ABC formation. Furthermore, ZEB2 haplo-insufficient Mowat Wilson syndrome (MWS) patients have decreased circulating ABCs in the blood. In Cd23Cre/+Zeb2fl/fl mice with impaired ABC formation, ABCs were dispensable for efficient humoral responses after Plasmodium sporozoite immunization but were required to control recrudescent blood-stage malaria. Immune phenotyping revealed that ABCs drive optimal T follicular helper (Tfh) cell formation and germinal center (GC) responses and they reside at the red/white pulp border likely permitting better access to pathogen antigens for presentation. Collectively, our study shows that ABC formation is dependent upon Zeb2, and these cells can limit recrudescent infection by sustaining GC reactions.
2024-02-09 | GSE213186 | GEO
Project description:Age/autoimmune-associated B cells (ABCs) are a T-bet dependent B cell subset, which accumulates prematurely in autoimmune settings. The molecular pathways that regulate ABCs in autoimmunity are largely unknown. The SWEF proteins include SWAP-70 and DEF6, a newly identified SLE risk variant. SWEF-deficient mice (double knock-out=DKO) develop a lupus like syndrome, which is accompanied by a marked expansion of ABCs. The accumulation of ABCs in DKO mice provided us with a unique opportunity to gain new insights into the molecular features that characterize the ABCs that prematurely expand in autoimmune conditions. Splenic Follicular B cells (FoB, B220+CD19+CD23+CD11c-CD11b-) and ABCs (B220+CD19+CD11c+CD11b+) were FACS sorted from >20 weeks old WT or DKO female mice and RNA-seq was employed to compare the transcriptome of DKO ABCs to that of FoB cells derived from either WT or DKO mice. Here we show that loss of SWEF proteins leads to altered gene expression in B cells independently of their differentiation state. In addition, a subset of genes was uniquely regulated in ABCs from DKO mice as compared to FoB cells from either WT or DKO mice. Ananlysis of the ATAC-seq experiment show that the ABCs that expand aberrantly in the DKO autoimmune setting exhibit a unique chromatin landscape and ABC-specific accessible loci displayed enrichment in AP-1/BATF, IRF, and T-bet binding motifs. Together our findings suggest that absence of SWEF proteins affects several key processes in ABCs. In particular, we observed alterations in a number of pathways involved in the control of cellular proliferation and inflammation, a finding that may play a crucial role in the premature accumulation of ABCs in DKOs and could distinguish them from non-autoimmune ABCs.
2018-03-01 | GSE99480 | GEO
Project description:Purpose: to identify the effects on the transcriptome of overexpressing ZFP36L1 in FO B cells
2017-03-01 | GSE79633 | GEO
Project description:Bacillus safensis FO-36b Genome Sequencing
| PRJNA162775 | ENA