Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Distinct Metabolic Requirements Regulate B Cell Activation and Germinal Center Responses

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE232660 | GEO | 2023/05/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Distinct Metabolic Requirements Regulate B Cell Activation and Germinal Center Responses

Project description:Distinct Metabolic Requirements Regulate B Cell Activation and Germinal Center Responses

| PRJNA973107 | ENA

αv Integrins regulate germinal center B cell responses through noncanonical autophagy.

Project description:Germinal centers (GCs) are major sites of clonal B cell expansion and generation of long-lived, high-affinity antibody responses to pathogens. Signaling through TLRs on B cells promotes many aspects of GC B cell responses, including affinity maturation, class switching, and differentiation into long-lived memory and plasma cells. A major challenge for effective vaccination is identifying strategies to specifically promote GC B cell responses. Here, we have identified a mechanism of regulation of GC B cell TLR signaling, mediated by αv integrins and noncanonical autophagy. Using B cell-specific αv-KO mice, we show that loss of αv-mediated TLR regulation increased GC B cell expansion, somatic hypermutation, class switching, and generation of long-lived plasma cells after immunization with virus-like particles (VLPs) or antigens associated with TLR ligand adjuvants. Furthermore, targeting αv-mediated regulation increased the magnitude and breadth of antibody responses to influenza virus vaccination. These data therefore identify a mechanism of regulation of GC B cells that can be targeted to enhance antibody responses to vaccination.

| S-EPMC6118577 | biostudies-literature

Bacterial infection disrupts established germinal center reactions through monocyte recruitment and impaired metabolic adaptation

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-02 | GSE188476 | GEO

mTORC1 and B cell survival signal regulate formation of memory precursors in the germinal center

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-13 | GSE147096 | GEO

Dynamic changes in E protein activity orchestrate germinal center and plasma cell development

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-12 | E-GEOD-72832 | biostudies-arrayexpress

Notch2-dependent DC2s mediate splenic germinal center responses.

Project description:CD4+ T follicular helper (TFH) cells support germinal center (GC) reactions promoting humoral immunity. Dendritic cell (DC) diversification into genetically distinct subsets allows for specialization in promoting responses against several types of pathogens. Whether any classical DC (cDC) subset is required for humoral immunity is unknown, however. We tested several genetic models that selectively ablate distinct DC subsets in mice for their impact on splenic GC reactions. We identified a requirement for Notch2-dependent cDC2s, but not Batf3-dependent cDC1s or Klf4-dependent cDC2s, in promoting TFH and GC B cell formation in response to sheep red blood cells and inactivated Listeria monocytogenes This effect was mediated independent of Il2ra and several Notch2-dependent genes expressed in cDC2s, including Stat4 and Havcr2 Notch2 signaling during cDC2 development also substantially reduced the efficiency of cDC2s for presentation of MHC class II-restricted antigens, limiting the strength of CD4 T cell activation. Together, these results demonstrate a nonredundant role for the Notch2-dependent cDC2 subset in supporting humoral immune responses.

| S-EPMC6196531 | biostudies-literature

Transcriptional regulation of germinal center B and plasma cell fates by dynamical control of IRF4

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-05-04 | E-GEOD-46608 | biostudies-arrayexpress

TFH cells progressively differentiate to regulate the germinal center response.

Project description:Germinal center (GC) B cells undergo affinity selection, which depends on interactions with CD4(+) follicular helper T cells (TFH cells). We found that TFH cells progressed through transcriptionally and functionally distinct stages and provided differential signals for GC regulation. They initially localized proximally to mutating B cells, secreted interleukin 21 (IL-21), induced expression of the transcription factor Bcl-6 and selected high-affinity B cell clones. As the GC response evolved, TFH cells extinguished IL-21 production and switched to IL-4 production, showed robust expression of the co-stimulatory molecule CD40L, and promoted the development of antibody-secreting B cells via upregulation of the transcription factor Blimp-1. Thus, TFH cells in the B cell follicle progressively differentiate through stages of localization, cytokine production and surface ligand expression to 'fine tune' the GC reaction.

| S-EPMC5030190 | biostudies-literature

Coordinated changes in glycosylation regulate the germinal center through CD22.

Project description:Germinal centers (GCs) are essential for antibody affinity maturation. GC B cells have a unique repertoire of cell surface glycans compared with naive B cells, yet functional roles for changes in glycosylation in the GC have yet to be ascribed. Detection of GCs by the antibody GL7 reflects a downregulation in ligands for CD22, an inhibitory co-receptor of the B cell receptor. To test a functional role for downregulation of CD22 ligands in the GC, we generate a mouse model that maintains CD22 ligands on GC B cells. With this model, we demonstrate that glycan remodeling plays a critical role in the maintenance of B cells in the GC. Sustained expression of CD22 ligands induces higher levels of apoptosis in GC B cells, reduces memory B cell and plasma cell output, and delays affinity maturation of antibodies. These defects are CD22 dependent, demonstrating that downregulation of CD22 ligands on B cells plays a critical function in the GC.

| S-EPMC9018098 | biostudies-literature

OBF1 and Oct factors control the germinal center transcriptional program

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-02 | GSE142040 | GEO