Impact of anti-CD40 treatment on mouse livers
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE159761 | GEO | 2021/10/25
REPOSITORIES: GEO
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Project description:Impact of anti-CD40 treatment on mouse livers
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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
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2004-02-16 | GSE1014 | GEO
Project description:Temporal analysis (60, 180, 360 min) of B cells treated with Anti-IgM alone, CD40 alone or Anti-IgM and CD40 (all in triplicates). Keywords: other
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Project description:To investigate the anti-tumor effect of agonistic anti-CD40, 4NQO-indued OSCC mice with agonistic anti-CD40.
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Project description:The interaction between the transmembrane glycoprotein surface receptor CD40 expressed by skin keratinocytes (KCs) and its T cell-expressed ligand CD154 was suggested to exacerbate inflammatory skin diseases. However, the full spectrum of CD40-mediated effects by KCs underlying this observation is unknown. Therefore, changes in gene expression after CD40 ligation of KCs were studied by microarrays. CD40-mediated activation for 2 hours stimulated the expression of a coordinated network of immune-involved genes strongly interconnected by IL8 and TNF, while after 24 hours anti-proliferative and anti-apoptotic genes were upregulated. CD40 ligation stimulated the production of chemokines that attracted lymphocytes and myeloid cells from peripheral blood mononuclear cells (PBMCs). Thus, CD40-mediated activation of KCs resulted in a highly coordinated response of genes required for the local development and sustainment of adaptive immune responses. The importance of this process was confirmed by a study on the effects of human papilloma virus (HPV) infection to the KCâs response to CD40 ligation. HPV infection clearly attenuated the magnitude of the response to CD40 ligation and consequently the KCâs capacity to attract PBMCs. The fact that HPV attenuates CD40 signalling in KCs indicates the importance of the CD40-CD154 immune pathway in boosting cellular immunity within epithelia. Total RNA from eight 72 hours 50 IU/ml IFNgamma pre-stimulated primary undifferentiated keratinocyte cultures, four uninfected and four HPV-positive, that were either left unstimulated, or stimulated for 2 hours with IFNgamma and Control- or CD40L-expressing L-cells (mouse fibroblasts), or stimulated for 24 hours with IFNgamma and Control- or CD40L-expressing L-cells. The stimulated samples were generated in duplo. 72 samples were generated in total.
2015-10-26 | E-GEOD-54181 | biostudies-arrayexpress
Project description:CD40-stimulating immunotherapy elicits potent anti-tumor responses, which are mainly T-cell dependent. Here, we have investigated how tumor endothelial cells respond to CD40-stimulating immunotherapy by isolating endothelial cells from B16.F10 melanoma in anti-CD40 treated or isotype treated mice followed by RNA-sequencing. Gene set enrichment analysis revealed an increase in interferon- related responses in tumor endothelial cells following anti-CD40 therapy. The immunosuppressive enzyme indoleamine 2, 3-dioxygenase 1 (IDO1) was preferentially expressed in endothelial cells, and it was up-regulated upon anti-CD40 treatment. IDO1 expression in tumor endothelium was positively correlated to T-cell infiltration and to increased expression of IFNγ in the tumor microenvironment. In vitro, endothelial cells up-regulated IDO1 in response to T-cell-derived IFNγ, but not in response to CD40-stimulation. Combining agonistic anti-CD40 therapy with the IDO1 inhibitor epacadostat delayed tumor growth and increased survival in B16.F10 tumor-bearing mice, which was associated with increased activation of tumor-infiltrating T-cells. Hereby, we have uncovered an immunosuppressive feedback mechanism, in which tumor vessels limit the efficacy of cancer immunotherapy by up-regulating IDO1 in response to T-cell activation.
2020-04-06 | GSE130679 | GEO
Project description:Murine B cells can be activated via the surface receptors TLR4 and CD40. For a global assessment of differences in gene expression between these two different modes of B cell activation a genome wide transcriptome analysis was performed. In order to dissect different gene expression profiles of B cells, activation was induced by LPS or LPS + anti-CD40 for 24h and 72h. Both activation states were compared to each other but also to naM-CM-/ve B cells. Gene expression profiles of naM-CM-/ve B cells, B cells activated with LPS and B cells activated with LPS + anti-CD40. Affymetrix MG 430 2.0 whole genome arrays were performed in quadruplicates for naM-CM-/ve B cells, B cells activated via TLR4 for 24 h and 72 h, and B cells activated via TLR4 + CD40 for 24 h and 72 h (20 arrays in total). To obtain genes significantly regulated upon stimulation with LPS, the expression profiles of naM-CM-/ve B cells, B cells activated with LPS for 24 h, and B cells activated with LPS for 72 h were compared to each other. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 M-BM-5g cRNA hybridized in quadruplicates for each of the five groups to the 20 GeneChip arrays: Group1 naM-CM-/ve B cells, Group2 LPS activated B cells 24h, Group3 LPS + anti-CD40 activated B cells 24h, Group4 LPS activated B cells 72h, and Group5 LPS + anti-CD40 activated B cells 72h. Access to PDF: http://dx.doi.org/10.1038/nature12979 All chips were imported into BioRetis (http://www.bioretis-analysis.de) and are open to the community now. If you want to obtain one or more lists of HPCDA significant genes you should click on a link of single chips (e.g. GSM879034) to get a description how to manage this.
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Project description:Treating ICB-resistant glioma with anti-CD40 and mitotic spindle checkpoint controller BAL101553 (lisavanbulin)
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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