Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling of bladder carcinoma T24 cells following CD40 activation by membrane-bound CD40L (mCD40L) compared to soluble CD40L (sCD40L)

ABSTRACT: We utilised the Affymetrix microarray analysis to compare the expression profiling of the CD40-positive bladder carcinoma T24 cells expressing mCD40L delivered by a replication-deficient adenovirus (RAdnCD40L) or treated with sCD40L (1µg/ml) for 24 hours

ORGANISM(S): Homo sapiens

PROVIDER: GSE98891 | GEO | 2020/01/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The T cell-DC CD40L-CD40 axis, but not platelet CD40L, drives atherosclerosis

Project description:Atherosclerosis, the underlying vascular cause of cardiovascular disease, has a strong inflammatory component. The co-stimulatory CD40-CD40 ligand (CD40L) signaling axis is a pivotal regulator of immune responses in atherosclerosis. However, therapeutic long-term inhibition of CD40L will severely compromise the immune system making it a non-viable treatment option. To circumvent this issue, cell-specific inhibition may present a better approach to target the CD40-CD40L axis. Therefore, we generated T cell and platelet-specific knockout mice for CD40L and apolipoprotein E, which were aged for 28 weeks to study their effects on immune status and atherosclerosis. Here, we show that T cell specific deficiency in CD40L signaling reduced plaque progression through hampered Th1 polarization as well as reduced antigen-dependent proliferation and oxLDL IgM production. DC-specific CD40 deficient mice displayed a similar phenotype. Platelet-specific CD40L deficiency, however, failed to decrease atherosclerosis, but ameliorated atherothrombosis. Together, our results illuminate the divergent cell-specific mechanisms of CD40-CD40L signaling in atherosclerosis, which may lead to advances in targeted therapies.

2021-03-16 | GSE145585 | GEO

Transcription profiling of human HUVEC T-cell (CD40L+) induced, anti-CD40-siRNA treated

Project description:The CD40-CD40L dyad seems to play a prominent role fostering the immune-inflammatory response triggered by endothelial cell (EC)-T cell interaction. To comprehensively delineate the involvement of CD40 (TNFRSF5) in EC activation, we combined RNAi-mediated CD40 knock-down with comparative genome-wide transcriptional profiling of EC in response to T cell. We report the initiation of a profound stress response in ECs upon CD40-CD40L engagement through early up-regulation, among others, of the major pro-inflammatory NFkB and MAPK/SAPK pathways and their associated transcription factors. Moreover, we have identified novel genes regulated through the CD40-CD40L interaction, and pathways previously unrecognized to be induced by CD40 signaling in ECs. Thus, we document a strong down-regulation of endothelial APLN by CD40-CD40L interaction, which could lead to vascular tone dysfunction in atherosclerotic lesions. Conversely, CD40-mediated up-regulation of the viral immune surveillance system, notably TLR3, IFIH1, RIG-I, and RNASEL, establishes a reverse link from adaptive to innate immunity in ECs. Moreover, systematic enrichment analysis substantiates endothelial CD40 involvement in the transcriptional regulation of gene networks associated with adhesion and motility, immunity, cell fate control, hemostasis and metabolism. Our study also highlights the potency and specificity of CD40 siRNA mediated inhibition, and the relevance of CD40 signaling pathways for anti-inflammatory therapeutic intervention. Experiment Overall Design: Time course experiment comparing endothelial gene expression profiling of CD40-silenced versus non-silenced cultured cells using RNA interference. Two independent experiments were performed where HUVECs were siRNA-transfected and co-cultured with Jurkat D1.1 for 4, 10, 16 h and harvested for RNA extraction. Technical dye swap duplicates were performed for each of the two biological replicates in all three time points.

2009-02-21 | E-GEOD-10601 | biostudies-arrayexpress

Time course gene expression profiling of T-cell (CD40L+) induced, anti-CD40-siRNA treated, HUVECs

Project description:The CD40-CD40L dyad seems to play a prominent role fostering the immune-inflammatory response triggered by endothelial cell (EC)-T cell interaction. To comprehensively delineate the involvement of CD40 (TNFRSF5) in EC activation, we combined RNAi-mediated CD40 knock-down with comparative genome-wide transcriptional profiling of EC in response to T cell. We report the initiation of a profound stress response in ECs upon CD40-CD40L engagement through early up-regulation, among others, of the major pro-inflammatory NFkB and MAPK/SAPK pathways and their associated transcription factors. Moreover, we have identified novel genes regulated through the CD40-CD40L interaction, and pathways previously unrecognized to be induced by CD40 signaling in ECs. Thus, we document a strong down-regulation of endothelial APLN by CD40-CD40L interaction, which could lead to vascular tone dysfunction in atherosclerotic lesions. Conversely, CD40-mediated up-regulation of the viral immune surveillance system, notably TLR3, IFIH1, RIG-I, and RNASEL, establishes a reverse link from adaptive to innate immunity in ECs. Moreover, systematic enrichment analysis substantiates endothelial CD40 involvement in the transcriptional regulation of gene networks associated with adhesion and motility, immunity, cell fate control, hemostasis and metabolism. Our study also highlights the potency and specificity of CD40 siRNA mediated inhibition, and the relevance of CD40 signaling pathways for anti-inflammatory therapeutic intervention. Keywords: treated vs. untreated comparison, time course

2009-02-10 | GSE10601 | GEO

Transcriptional effects of soluble CD40 ligand on human immature dendritic cells

Project description:We performed microarray analysis of sCD40L-stimulated iDC to derive a signature of CD40 activation. Human monocytes from normal healthy donors were differentiated to iDCs with GM-CSF and IL4. FACS analysis demonstrated the immature status of these cells, illustrated by low expression of CD80, CD40, and CD86. We confirmed that sCD40L induces the maturation of DCs, characterized by higher expression of CD80, HLA-DR, CD86, CD83 and CD40 and secretion of pro-inflammatory cytokines at 24hr post-stimulation. Cells were harvested at 1, 3 and 24hr post-stimulation for microarray analysis.

2017-06-08 | GSE85544 | GEO

CD40L membrane retention enhances the immunostimulatory effects of CD40 ligation.

Project description: Not available

| S-EPMC6962220 | biostudies-literature

Difference of DNA methylation and Chromatin accessibility of T24 SP cell and T24 NSP cell

Project description:Difference of DNA methylation and Chromatin accessibility of T24 SP cell and T24 NSP cell

2020-01-30 | GSE130641 | GEO

T cell cancer therapy requires CD40-CD40L activation of TNFα-iNOS-producing dendritic cells

Project description:The effectiveness of new cancer therapies such as checkpoint blockade and adoptive cell transfer of activated anti-tumor T cells requires overcoming immunosuppressive tumor microenvironments. We found that the activation of tumor-infiltrating myeloid cells to produce local nitric oxide is a prerequisite for adoptively transferred CD8+ cytotoxic T cells to destroy tumors. These myeloid cells are phenotypically similar to ‘Tip-DCs’ or nitric oxide- and TNFα-producing dendritic cells. The nitric oxide-dependent killing was tempered by coincident arginase 1 expression, which competes with iNOS for arginine, the substrate for nitric oxide production. Depletion of immunosuppressive CSF-1R-dependent arginase 1+ myeloid cells enhanced nitric oxide-dependent tumor killing. Tumor killing via iNOS was independent of the microbiota but dependent on the CD40-CD40L pathway and, in part, lymphotoxin alpha. We extended our findings in mice to uncover a strong correlation between iNOS, CD40 and TNF expression and survival in colorectal cancer patients. Our results identify a network of anti-tumor targets to boost the efficacy of cancer immunotherapies.

2016-09-14 | GSE74427 | GEO

The T cell-DC CD40L-CD40 axis, but not platelet CD40L, drives atherosclerosis

Project description:The T cell-DC CD40L-CD40 axis, but not platelet CD40L, drives atherosclerosis

| PRJNA607676 | ENA

Transcriptional effects of soluble CD40 ligand on human naïve B cells

Project description:We performed microarray analysis to derive gene signatures down-stream of soluble CD40 ligand stimulation in human naive B cells. Naïve B cells were purified from healthy donor PBMC using negative selection beads (Miltenyi) and cultured with sCD40L at 2.5ug/ml for 6hr before microarray analysis. In the same study, cells were also harvested at day 5 post-stimulation to confirm sCD40L-induced B cell activation and proliferation. FACS analysis confirmed soluble CD40L induced up-regulation of CD86 and CD69 at 24hr. B cell proliferation was measured at day 4 post-stimulation by EdU incorporation.

2017-06-08 | GSE85543 | GEO

Analysis of gene expression change between ectopic expression SOX2 in T24 bladder cancer cells.

Project description:We collected total RNA from both T24-Ctrl and T24-SOX2 and examined mRNA expression profile, comprehensively.

2020-02-25 | GSE145826 | GEO