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Genes regulated by T cell and B cell derived TNF in naive lymph nodes

ABSTRACT: We present a RNA microarray analysis of RNA`s extracted from naive mesenterial lymph nodes of mice with specific inactivation of tumor necrosis factor only in B cells (B-TNf mice) or in T- and B-cells (TB-TNF mice). Several genes are cooperatively regulated by T cell derived and B cell derived TNF Keywords: cell type comparison design

ORGANISM(S): Mus musculus

PROVIDER: GSE8610 | GEO | 2010/12/07

SECONDARY ACCESSION(S): PRJNA101781

REPOSITORIES: GEO

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Genes regulated by T cell and B cell derived TNF in naive lymph nodes

Project description:We present a RNA microarray analysis of RNA`s extracted from naive mesenterial lymph nodes of mice with specific inactivation of tumor necrosis factor only in B cells (B-TNf mice) or in T- and B-cells (TB-TNF mice). Several genes are cooperatively regulated by T cell derived and B cell derived TNF Keywords: cell type comparison design For 1 independent sample 3 mice of one genotype have been sacrificed, mesenterial lymph nodes were isolated and pooled together. Lymph nodes were immediately frozen in luquid N2 and RNA was prepared using Tri-reagent. RNA was precipitated with isopropanol, washed with 70% ethanol and dissolved in DEPC dH2O.

2010-12-07 | E-GEOD-8610 | biostudies-arrayexpress

Single Cell Transcriptomic Analysis of Popliteal Lymph Nodes from TNF-Tg Mice with Early and Advanced Inflammatory-Erosive Arthritis

Project description:Immune cell dynamics in lymph nodes downstream of inflamed joints are associated with inflammatory-erosive arthritis in both tumor necrosis factor transgenic (TNF-Tg) mice and rheumatoid arthritis (RA) patients. In TNF-Tg mice, "Early" stages of arthritis are related to dramatic PLN "Expansion" with increases in joint-draining popliteal lymph node (PLN) volume and fluid flow, while CD21-high / CD23+ B-cells in inflamed nodes (Bin cells) accumulate in the PLN follicles. Onset of "Advanced" inflammatory-erosive arthritis is related to a PLN "Collapse" where fluid flow is reduced as Bin cells translocate from the PLN follicles into the sinuses and are thought to mechanically inhibit lymphatic drainage. Through single-cell RNA-sequencing, we aimed to evaluate changes in PLN immune cell populations during Early and Advanced arthritis to determine mechanisms mediating the Bin cell translocation and the relationship with arthritic progession in the afferent joints.

2023-08-14 | GSE211124 | GEO

Spatial Transcriptomics of Joint-Draining Popliteal Lymph Nodes from Wild-type and TNF-Tg Mice with Early and Advanced Inflammatory-Erosive Arthritis

Project description:Lymphatic dysfunction is an integral aspect of rheumatoid arthritis (RA) pathogenesis. During "Early" arthritis in tumor necrosis factor transgenic (TNF-Tg) mice, the joint-draining popliteal lymph nodes (PLNs) dramatically expand in volume. After a prolonged expansion phase, at ~8-months-old the PLNs stochastically collapse with reduced bone volume and associated onset of "Advanced" inflammatory-erosive arthritis in affected joints. Through this pathologic process, B-cells are known to translocate into the PLN sinuses. Bulk tissue approaches (i.e. bulk genomics, flow cytometry, and ex vivo cell cultures) have been insufficient to specifically evaluate the transcriptional changes of B-cells within the sinuses of TNF-Tg PLNs. Thus, we utilized spatial transcriptomics technology to evaluate transcriptional changes in sinus B-cells and the functional genomic relationships with arthritic severity.

2023-08-14 | GSE195598 | GEO

Differential protein secretome induced by TNF-alpha

Project description:Endothelial-mesenchymal-transition (EndMT) is an important source of cancer-associated fibroblasts (CAFs), which are known to facilitate tumor progression. We have previously shown that EndMT is present in pancreatic tumors and that deficiency of the Tie1 receptor induces EndMT in human endothelial cells. Pancreatic tumors are characterized by the presence of tumor necrosis factor-α (TNF-α). We now show that TNF-α strongly induces human endothelial cells to undergo EndMT. In order to know the secretory feature of cells which undergo EndMT by TNF-α, we conducted a comparative analysis of HMVEC secretome treated or not for 24h and 48h with TNF-α. Secretome study shows that cells treated with TNF-α have an important fibroblast-like secretory capacity, and a proinflamatory signature. Moreover, Ingenuity Pathway Analysis (IPA) shows that pathways implicated in migration, inflammation and fibrosis are predicted to be activated and that necrosis and apoptosis pathways are inhibited. Accordingly cell survival, viability and cycle progression are activated. We show that TNF-α- treated cells secrete proteins related to 16 protumoral pathways, confirming their fibroblastic characteristic. Finally, among the predicted upstream regulators activated, IPA analysis shows that, TNFSF12 and its receptor are present at hight levels in PDAC patients. Altogether these results show the fibroblastic characteristic of treated cells and demonstrate that TNF-α induces CAFs.

2021-09-08 | PXD014488 | Pride

Risk of tuberculosis in Korean inflammatory bowel disease patients treated with Tumor Necrosis Factor-a (TNF-a) blockers

Project description:Primary outcome(s): Quantification of the incidence rate of TB in IBD patients treated with TNF-a blockers and compared that with general population rates Study Design: Observational Study Model : Cohort, Time Perspective : Retrospective, Enrollment : 1000, Biospecimen Retention : Not collect nor Archive

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Gene expression profiling in epidydimal fat from wild-type and macrophage-derived TNF-α deficient mice.

Project description:The pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-α), has been suggested to be a key factor in the induction of obesity-associated metabolic dysfunction. However, the role that macrophage-derived TNF-α has on regulating metabolic perturbations in obesity is not completely understood. Therefore, we utilized the TNF-αFlox/FLox (F/F), LyzMcre+/- mouse model to determine the impact that macrophage TNF-α deletion has on the development of high-fat-diet (HFD)-induced obesity.

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Cholesterol and TNF-induced transcriptomic changes in Mus musculus aortic smooth muscle cells

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Hi-C analysis in TNF-alpha-stimulated human umblical vein endothelial cells (HUVECs)

Project description:Lysine 9 di-methylation and lysine 27 tri-methylation of histone H3 (H3K9me2 and H3K27me3) are mostly linked to gene repression. However, functions of repressive histone methylation dynamics during inflammatory responses remain poorly understood. Here, we show that lysine demethylase 7A (KDM7A) and 6A (UTX) are rapidly transported to nuclear factor kappa-B (NF-κB) related elements in human endothelial cells in response to tumor necrosis factor (TNF)-α. KDM7A and UTX demethylate H3K9me2 and H3K27me3, respectively, and cooperatively activate NF-κB dependent inflammatory genes. Furthermore, using both in situ Hi-C and other 3C based technology, loops between super enhancers (SEs) are newly formed following TNF-α-stimuli at NF-κB-dependent inflammatory loci where KDM7A- and UTX-recruitment coincide. Collectively, these findings suggest that erasing of repressive histone marks by KDM7A and UTX within NF-κB-related elements might functionally associate with formation of SE-SE three-dimensional interactions and could be a cue signal during inflammatory responses in human endothelial cells.

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Phosphoproteome profiling uncovers a key role for CDKs in TNF signaling

Project description:Tumor necrosis factor (TNF) is one of the few cytokines successfully targeted by therapies against inflammatory diseases. However, blocking this well studied and pleiotropic ligand can cause dramatic side-effects. We reasoned that a systems-level proteomic analysis of TNF signaling could dissect its diverse functions and offer a base for developing more targeted therapies. Combining phosphoproteomics time course experiments with spatial and kinase inhibitor analysis clusters phosphorylations into functional modules. The majority of regulated phosphorylations could be assigned to an upstream kinase by inhibiting master kinases and spatial proteomics revealed phosphorylation-dependent translocations of hundreds of proteins upon TNF stimulation. Phosphoproteome analysis of TNF-induced apoptosis and necroptosis revealed a key role for transcriptional cyclin-dependent kinase (CDK) activity to promote cytokine production and prevent excessive cell death downstream of the TNF signaling receptor. Our comprehensive interrogation of TNF induced pathways and sites can be explored at http://tnfviewer.biochem.mpg.de/.

2021-10-11 | PXD021366 | Pride

Gene expression profiling of cardiac-specific overexpression of TNF-α in Des-/- myocardium

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