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CD40L and TNF both activate the classical NF-kappaB pathway, which is not required for the CD40L induced alternative pathway in endothelial cells

ABSTRACT: CD40L and TNF both activate the classical NF-kappaB pathway, which is not required for the CD40L induced alternative pathway in endothelial cells

PROVIDER: PRJNA420097 | ENA |

REPOSITORIES: ENA

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CD40L and TNF both activate the classical NF-kappaB pathway, which is not required for the CD40L induced alternative pathway in endothelial cells

Project description:Here, we have compared the gene expression repertoire of CD40L (CD154) and TNF stimulated HUVEC and report that unexpectedly, apart from a stronger response to TNF, no major qualitative differences could be observed. This applies for the period of up to six hours, a time where the alternative pathway has already been activated. Analysis of the early events after receptor engagement revealed that both TNF and CD40L activate the classical NF-kappaB pathway, and confirm activation of the alternative by the latter. Furthermore, using genetic and pharmacological inhibition of the classical pathway we show that activation of the alternative occurs independently of the former. This reveals novel insights into NF- kappaB signaling by CD40L and TNF in endothelial cells

2017-11-29 | GSE107453 | GEO

Classical and/or alternative NF-kB pathway activation in multiple myeloma pathogenesis

Project description:Mutations involving the NFKB pathway are present in at least 17% of multiple myeloma (MM) tumors and 40% of MM cell lines (MMCL). These mutations, which are thought to be progression events, enable MM tumors to become less dependent on extrinsic bone marrow signals that activate NFKB. Studies on a panel of 50 MMCL provide some clarification of the mechanisms through which these mutations act and the significance of classical vs alternative activation of NFKB. First, only one mutation (NFKB2) selectively activates the alternative pathway, whereas several mutations (CYLD, NFKB1, TACI) selectively activate the classical pathway. However, most mutations affecting NIK level (NIK, TRAF2, TRAF3, cIAP1&2, CD40) activate the alternative but often both pathways. Second, we confirm the critical role of TRAF2 in regulating NIK degradation, whereas TRAF3 enhances but is not essential for cIAP1/2-mediated proteosomal degradation of NIK in MM. Third, using transfection to selectively activate the classical or alternative NFKB pathways, we show virtually identical changes in gene expression in one MMCL, whereas the changes are similar albeit non-identical in a second MMCL. Together, our results suggest that MM tumors can achieve increased autonomy from the bone marrow microenvironment by mutations that activate either NFKB pathway.

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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

Expression data from Human CD40L+ Tcells

Project description:To assess the nature of CD8+CD40L+ memory Tcells, we compared the gene expression to CD8+CD40L- and CD4+ counterparts, and found similarities in expression of genes encoding cytokines PBMCs were isolated from five healthy donors. The cells were stimulated with PMA/Ionomycin for 6 h, and subsequently sorted into the CD4+CD45RA-CD40L+, CD8+CD45RA-CD40L-, CD8+CD45RA-CD40L+ populations by FACS-sort

2013-08-05 | E-GEOD-44126 | biostudies-arrayexpress

Expression data from Human CD40L+ Tcells

Project description:To assess the nature of CD8+CD40L+ memory Tcells, we compared the gene expression to CD8+CD40L- and CD4+ counterparts, and found similarities in expression of genes encoding cytokines. PBMCs were isolated from five healthy donors. The cells were stimulated with PMA/Ionomycin for 6 h, and subsequently sorted into the CD4+CD45RA-CD40L+, CD8+CD45RA-CD40L-, CD8+CD45RA-CD40L+ populations by FACS-sort.

2019-01-30 | E-MTAB-1497 | biostudies-arrayexpress

Expression data from Human CD40L+ Tcells

2013-08-05 | GSE44126 | 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

Primary Human B-cell Temporal Response to CD40L Stimulation

Project description:RNAseq was used to identify primary human B-cell responses to CD40L stimulation. Primary human peripheral blood B-cells were isolated by negative selection and then subjected to 0, 1 or 18 hours of mega-CD40L stimulation at 50 ng/ml.

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Expression data of human tonsil centroblasts (CB) cultured w/o CD40L + IL-21

Project description:CD40L and IL-21 are major contributors to the transcriptional emergency of PC identify genes in committed B cells. In order to decipher specific CD40L- and IL21-targeted genes, fresly purified human tonsil centroblasts (n=6) were cultured for 3 hours in presence or not of CD40L and IL-21 before transciptome analysis were performed.

2019-08-23 | GSE136248 | GEO

NFkB in multiple myeloma - EJM IkBa super-repressor

Project description:Mechanisms of constitutive NF-kappaB signaling in multiple myeloma are unknown. An inhibitor of IkappaB kinase beta (IKKbeta), targeting the classical NF-kappaB pathway, was lethal to many myeloma cell lines. Several had elevated expression of NIK due to genomic alterations or enhanced protein stability while others had inactivating mutations or deletion of TRAF3. Both abnormalities triggered the classical and alternative NF-kappaB pathways. A majority of primary myeloma patient samples and cell lines had elevated NF-kappaB target gene expression, often associated with genetic and epigenetic alteration of NIK, TRAF3, CYLD, BIRC2/BIRC3, CD40, NFKB1, and NFKB2. These genetic and functional data demonstrate that addiction to the NF-kappaB pathway is a frequent feature of myeloma and suggest that IKKbeta inhibitors hold promise for the treatment of this disease. Keywords: time series design

2007-10-29 | GSE8477 | GEO

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