B cell response to Anti-IgM and CD40 treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE1019 | GEO | 2004/02/13
SECONDARY ACCESSION(S): PRJNA90255
REPOSITORIES: GEO
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Project description:Temporal analysis (60, 180, 360 min) of B cells treated with Anti-IgM alone, terbutaline alone or Anti-IgM and terbutaline (all in triplicates). Keywords: other
2004-02-13 | GSE1021 | GEO
Project description:Temporal analysis (60, 180, 360 min) of B cells treated with Anti-IgM alone, ELC alone or Anti-IgM and ELC (all in triplicates). Keywords: other
2004-02-13 | GSE1020 | GEO
Project description:Temporal analysis (60, 180, 360 min) of B cells treated with either: CD40 Anti-IgM ELC IL4 Lipopolysaccharide Terbutaline CD40 and IL4 CD40 and Lipopolysaccharide CD40 and Anti-IgM Anti-IgM and ELC Anti-IgM and Terbutaline ELC and Lipopolysaccharide This SuperSeries is composed of the SubSeries listed below.
2004-02-16 | GSE1014 | GEO
Project description:Temporal analysis (60, 180, 360 min) of B cells treated with CD40 alone, IL4 alone or CD40 and IL4 (all in triplicates). Keywords: other
2004-02-13 | GSE1023 | GEO
Project description:Temporal analysis (60, 180, 360 min) of B cells treated with CD40 alone, lipopolysaccharide alone or CD40 and lipopolysaccharide (all in triplicates). Keywords: other
2004-02-13 | GSE1022 | GEO
Project description:Temporal analysis (60, 180, 360 min) of B cells treated with either: CD40 Anti-IgM ELC IL4 Lipopolysaccharide Terbutaline CD40 and IL4 CD40 and Lipopolysaccharide CD40 and Anti-IgM Anti-IgM and ELC Anti-IgM and Terbutaline ELC and Lipopolysaccharide This SuperSeries is composed of the following subset Series: GSE1019: B cell response to Anti-IgM and CD40 treatment GSE1020: B cell response to Anti-IgM and ELC treatment GSE1021: B cell response to Anti-IgM and terbutaline treatment GSE1022: B cell response to CD40 and lipopolysaccharide treatment GSE1023: B cell response to CD40 and IL4 treatment GSE1024: B cell response to ELC and lipopolysaccharide treatment Refer to individual Series
2010-06-09 | E-GEOD-1014 | biostudies-arrayexpress
Project description:Temporal analysis (60, 180, 360 min) of B cells treated with ELC alone, lipopolysaccharide alone or ELC and lipopolysaccharide (all in triplicates). Keywords: other
2004-02-13 | GSE1024 | GEO
Project description:Background: The co-stimulatory CD40-CD40L dyad is an important driver of atherosclerosis. CD40 exerts divergent, cell-specific roles, which differentially impact atherogenesis. Objectives: We here investigate the role of the most prominent CD40-expressing cell-type, the B-cell, in atherosclerosis. Methods: B-cell subset specific CD40-expression of patients with mild and severe coronary artery disease (CAD) was determined by mass-cytometry and correlated to CAD severity. Underlying mechanisms were elucidated using B-cell CD40-deficient CD19Cre-CD40flfl-ApoE-/-(CD40BKO) mice and control littermates (CD40BWT). Results: Patients with severe CAD had similar CD40 expression levels on most B-cell subsets but showed a profound decrease in CD40 on putative B1 cells. This was associated with increased atherosclerotic plaque burden and decreased plaque fibrosis. Likewise, CD40BKO mice exhibited an increased plaque area and more advanced staging of atherosclerosis. Absence of CD40 on B-cells caused a decrease in immunoglobulin (Ig) producing cells, including germinal center-, plasma-, but especially B1 cells, thereby reducing levels of (anti-ox/MDA-LDL) IgG and protective (anti-ox/MDA-LDL) IgM. Transcriptomics analysis revealed that the absence of CD40 on B1b cells caused altered gene expression pathways related to lipid uptake (Cd36, Ldlr), cellular stress and metabolism (Nr4a1, Hif1a), and cell death (Naip5/6, Ccnd2). Indeed, in vitro analysis showed that B1bCD40KO cells took up excessive amounts of ac/oxLDL, exhibited defective BCR signaling, and were prone to apoptosis, especially in hyperlipidemic conditions. Transfer of wild-type B1b cells in CD40BKO mice prevented the increase in atherosclerosis. Conclusions: Patients with severe CAD had similar CD40 expression levels on most B-cell subsets but showed a profound decrease in CD40 on putative B1 cells. This was associated with increased atherosclerotic plaque burden and decreased plaque fibrosis. Likewise, CD40BKO mice exhibited an increased plaque area and more advanced staging of atherosclerosis. Absence of CD40 on B-cells caused a decrease in immunoglobulin (Ig) producing cells, including germinal center-, plasma-, but especially B1 cells, thereby reducing levels of (anti-ox/MDA-LDL) IgG and protective (anti-ox/MDA-LDL) IgM. Transcriptomics analysis revealed that the absence of CD40 on B1b cells caused altered gene expression pathways related to lipid uptake (Cd36, Ldlr), cellular stress and metabolism (Nr4a1, Hif1a), and cell death (Naip5/6, Ccnd2). Indeed, in vitro analysis showed that B1bCD40KO cells took up excessive amounts of ac/oxLDL, exhibited defective BCR signaling, and were prone to apoptosis, especially in hyperlipidemic conditions. Transfer of wild-type B1b cells in CD40BKO mice prevented the increase in atherosclerosis.
2024-10-19 | GSE186134 | GEO
Project description:To simulate transient B cell activation that is the likely initiator of T-dependent responses, we examined the molecular and functional consequences of a single-round of immunoglobulin M (IgM) signaling. This form of activation triggered early cytosolic signaling and transcription factor NF-kB activation indistinguishably from conventional continuous IgM cross-linking, but did not induce G1 progression. However, single-round IgM signaling changed the expression of chemokine and chemokine receptor genes implicated in initiating T-dependent responses, as well as accentuated responsiveness to CD40 signaling. Several features of single-round IgM signaling in vitro were recapitulated in B cells after short-term exposure to antigen in vivo. We propose that transient BCR signals prime B cells to receive T cell help by increasing the probability of B-T encounter and creating a cellular environment that is hyper-responsive to CD40 signaling. Primary B lymphocytes were isolated using Auto-MACS (Miltenyi Biotec) by negative selection. B cell purity was 90-95% based on flow cytometric analysis with CD19 staining. Purified B cells (2x10^6/ml) were cultured in RPMI 1640 supplemented with 10% heat-inactivated FBS, 55nM beta-mercaptoethanol, 2mM L-glutamine and 100IU penicillin and 100ug/ml streptomycin at 37degrees C. For pulsed anti-IgM treatment experiments, B cells were incubated with 10ug/ml goat anti-mouse IgM F(abâ)2 (Jackson ImmunoResearch Laboratories) at 4 degrees C for 30 min. Unbound anti-IgM was removed from the medium by washing and centrifuging the cells at 4 degrees C. The cells were resuspended in chilled complete medium and shifted to 37 degrees C by placing in an incubator or in water-bath. For continuous anti-IgM treatment experiments, B cells were stimulated with 10ug/ml anti-IgM at 4 degrees C for 30 min, then incubated at 37 degrees C.
2010-06-08 | E-GEOD-20477 | biostudies-arrayexpress
Project description:Purpose: To gain insight into both similarities and differences in the gene expression programs induced by IL-21R, BCR and CD40 signals, we performed RNA-seq on both GCBC and NBC that had been stimulated for either 2h or 4h with IL-21, CD40 ligation, BCR ligation, or combinations of these. Methods : Purified GCBC from d14 NP-CGG immunized MEG mice and NBC from naïve MEG mice were warmed at 37C for 30 minutes and then stimulated with 10ng/mL IL-21, 20μg/ml ⍺-IgM or 2.5μg/mL ⍺-CD40 (prepared as tetramer) alone or combined IL21/⍺-CD40 or ⍺-IgM/⍺-CD40 for 2 and 4 hours. After stimulation, cells were processed for RNA isolation using QIAshredder columns (Qiagen) and the RNeasy Plus Mini Kit (Qiagen) following the manufacturer’s instructions. Samples were sequenced using Illumina NextSeq 500 with 75 bp paired-end reads and aligned to the mm10 genome using the STAR aligner (Dobin et al., 2013). Gene-level counts were determined using featureCounts (Liao et al., 2014), and raw counts were quantile normalized to each other for differential expression using the voom method (Law et al., 2014) in the Limma R package (Ritchie et al., 2015). For normalization of the datasets, the Quantile method was used. Results: Like BCR and CD40 signals, IL-21R plus CD40 signals also synergize to induce c-Myc in GCBC. However, IL-21R plus CD40 stimulation differentially affects GCBC fate compared to BCR plus CD40 ligation—engaging unique molecular mechanisms
2023-02-16 | GSE197662 | GEO