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CD40-activation of human B cells

ABSTRACT: Antibody-independent effector functions of B cells, such as antigen presentation and cytokine production, have been shown to play an important role in a variety of immune-mediated conditions such as autoimmune diseases, transplant rejection and graft-versus-host disease. Therapeutic strategies, which interfere with B cell activation could therefore be a useful addition to the current immunosuppressive armamentarium. CD40 is one of the strongest activation stimuli for B cells. The aim of this study was to characterise the gene expression changes that occurr after B cell activation via CD40. Purified B cells isolated from PBMCs from four donors were compared to B cells which

ORGANISM(S): Homo sapiens

SUBMITTER: Alexander Shimabukuro-Vornhagen

PROVIDER: E-GEOD-54017 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression of murine B cells activated via TLR4 or TLR4 + CD40: 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.

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.

2014-02-24 | E-GEOD-35998 | biostudies-arrayexpress

CD40-mediated amplification of local immunity by keratinocytes in impaired by HPV

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

CD40-activation of human B cells

Project description:Antibody-independent effector functions of B cells, such as antigen presentation and cytokine production, have been shown to play an important role in a variety of immune-mediated conditions such as autoimmune diseases, transplant rejection and graft-versus-host disease. Therapeutic strategies, which interfere with B cell activation could therefore be a useful addition to the current immunosuppressive armamentarium. CD40 is one of the strongest activation stimuli for B cells. The aim of this study was to characterise the gene expression changes that occurr after B cell activation via CD40.

2014-01-14 | GSE54017 | GEO

Time course and dose response analysis of gene expression in BCR or CD40-stimulated DT40 B cell

Project description:Gene Expression dynamics is important information. To know IKK- or ERK-dependent B cell receptor- or CD40-induced gene expression dynamics, we performed the time course and dose response analysis in wild type or MEK inhibitor treated or IKKbeta inactive DT40 B cells. Two replicated samples were analysed. Unstimulated cells (T0) were control. WT cells or MEK Inh. (MEK inhibitor;U0126 5mM, 30min pretreated) or IKKbetaSA (S176/181A knock-in) Cells were stimulated with 0.1, 1, 10 Âµg/ml of anti-IgM (M4) or 1, 3, 6 Âµg/ml of CD40ligand (CD40L) for 0, 15, 30, 45, 60 or 90min.

2014-08-01 | E-GEOD-59002 | biostudies-arrayexpress

Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells. B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells and cultures with mitogens in vitro. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.

2015-11-01 | E-GEOD-74287 | biostudies-arrayexpress

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

RNAseq data from in vitro-stimulated (6 hours) murine relafl/flCD19-Cre and CD19-Cre splenic B cells purified by magnetic cell separation (RELA)

Project description:RNAseq analysis of CD40 + IgM in vitro-stimulated (6 hours) murine relafl/flCD19-Cre (furtheron designated as RELA) and CD19-Cre (furtheron designated as WT) splenic B cells identifies genes regulated by the transcription factor RELA in activated B cells. Splenic B cells from 12-week old relafl/flCD19-Cre and CD19-Cre littermate mice were isolated by magnetic cell separation from splenic mononuclear cells and stimulated in vitro for 6 hours with anti-CD40 and anti-IgM. RNA was isolated and submitted for RNA-sequencing on an Illumina HiSeq2000 instrument for 30 million single-ended reads.

2014-07-15 | E-GEOD-58972 | biostudies-arrayexpress

RNAseq data from in vitro-stimulated (6 hours) murine relfl/flCD19-Cre and CD19-Cre splenic B cells purified by magnetic cell separation (REL6)

Project description:RNAseq analysis of CD40 + IgM in vitro-stimulated (6 hours) murine relfl/flCD19-Cre (furtheron designated as REL) and CD19-Cre (furtheron designated as WT) splenic B cells identifies genes regulated by the transcription factor c-REL in activated B cells. Splenic B cells from 12-week old relfl/flCD19-Cre and CD19-Cre littermate mice were isolated by magnetic cell separation from splenic mononuclear cells and stimulated in vitro for 6 hours with anti-CD40 and anti-IgM. RNA was isolated and submitted for RNA-sequencing on an Illumina HiSeq2000 instrument for 30 million single-ended reads.

2014-07-15 | E-GEOD-58971 | biostudies-arrayexpress

RNAseq data from in vitro-stimulated (24 hours) murine relfl/flCD19-Cre and CD19-Cre splenic B cells purified by magnetic cell separation.

Project description:RNAseq analysis of CD40 + IgM in vitro-stimulated (24 hours) murine relfl/flCD19-Cre (furtheron designated as REL) and CD19-Cre (furtheron designated as WT) splenic B cells identifies genes regulated by the transcription factor c-REL in activated B cells. Splenic B cells from 12-week old relfl/flCD19-Cre and CD19-Cre littermate mice were isolated by magnetic cell separation from splenic mononuclear cells and stimulated in vitro for 24 hours with anti-CD40 and anti-IgM. RNA was isolated and submitted for RNA-sequencing on an Illumina HiSeq2000 instrument for 30 million single-ended reads.

2014-07-15 | E-GEOD-58973 | biostudies-arrayexpress

Genetically-driven target tissue over-expression of CD40: A novel mechanism in autoimmune disease

Project description:The CD40 gene, an important immune regulatory gene, is also expressed and functional on non-myeloid derived cells, many of which are targets for tissue specific autoimmune diseases, including d thyroid follicular cells in Graves’ disease (GD). Whether target tissue CD40 expression plays a role in autoimmune disease etiology has yet to be determined. Here we show for the first time, that target-tissue over-expression of CD40 plays a key role in the etiology of autoimmunity. Using a murine model of GD, we demonstrated that thyroidal CD40 over-expression augmented the production of thyroid specific antibodies, resulting in more severe experimental autoimmune Graves’ disease (EAGD), whereas deletion of thyroidal CD40 suppressed disease. Using transcriptome and immune-pathway analyses we showed that in both EAGD mouse thyroids and human primary thyrocytes, CD40 mediates this effect by activating downstream cytokines and chemokines, most notably IL-6. To translate these findings into therapy, we blocked IL-6 during EAGD induction in the setting of thyroidal CD40 over-expression, and showed decreased levels of TSHR stimulating antibodies and frequency of disease. We conclude that target tissue over-expression of CD40 plays a key role in the etiology of organ specific autoimmune disease. CD40 in Thyroid Autoimmunity: 1) Incubation of human thyroid cells with G28.5, a CD40 stimulating antibody, and purification of RNA, conversion to cDNA, measurement of mRNA expression using RNAseq. 2) Removal of thyroid tissues from CD40 over-expressing transgenic mice and wild type mice, purification of RNA, conversion to cDNA measurement of mRNA expression using RNAseq.

2012-10-03 | E-GEOD-39081 | biostudies-arrayexpress

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