Project description:MDA-MB-231 cells were treated with PBS, LPS, IL1b, TNFa, IL6, and TGFb respectively and expression profile were assayed by Arraystar human lncRNA array 2.0

2015-03-01 | GSE57539 | GEO

lncRNA and mRNA expression of cytokine treated MDA-MB-231 cells

Project description:MDA-MB-231 cells were treated with PBS, LPS, IL1b, TNFa, IL6, and TGFb respectively and expression profile were assayed by Arraystar human lncRNA array 2.0 We designed this experiment to screen for lncRNAs whose expressions are responsive to inflammatory stimuli.

2015-03-01 | E-GEOD-57539 | biostudies-arrayexpress

MDMs Solvent, AA, IL6, AA+IL6

Project description:MDMs Solvent, AA, IL6, AA+IL6

| PRJEB36942 | ENA

Genome-wide analysis of the transcriptional profile of IL1b/TNFa-treated and EAE astrocytes in B6 mice.

Project description:Genome-wide analysis of the transcriptional profile of IL1b/TNFa-treated and EAE astrocytes in B6 mice.

| PRJNA565156 | ENA

Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6

Project description:Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6

| PRJNA961207 | ENA

A chromatin-regulated biphasic circuit coordinates IL1B-mediated inflammation

Project description:Inflammation is characterized by a biphasic cycle consisting initially of a pro-inflammatory phase which is subsequently resolved by anti-inflammatory processes. The coordination of these two disparate states needs to be highly controlled, suggesting that the regulation of the cytokines that drive these processes are intimately linked. Interleukin-1 beta (IL1B) is a master regulator of pro-inflammation and is encoded within the same topologically associated domain (TAD) as interleukin-37 (IL37). IL37 has recently emerged as a powerful anti-inflammatory cytokine which diametrically opposes the function of IL1B. Within this TAD, we identified a novel long non-coding RNA called AMANZI which negatively regulates IL1B expression and trained immunity through the induction of IL37 transcription. We found that the activation of IL37 occurs through the formation of a dynamic long-range chromatin contact that leads to the temporal delay of anti-inflammatory responses. The common variant rs16944 present in AMANZI augments this regulatory circuit, predisposing individuals to enhanced pro-inflammation or immunosuppression. Our work illuminates a chromatin-mediated biphasic circuit coordinating expression of IL1B and IL37, thereby regulating two functionally opposed states of inflammation from within a single TAD.

2023-10-27 | PXD045971 | Pride

Autocrine IL6 activates the STAT3-DNMT axis to silence the TNFa-RIP1 necroptosis pathway to sustain myeloid-derived suppressor cell survival and accumulation

Project description:Massive accumulation of myeloid-derived suppressor cells (MDSCs) is a hallmark of cancer. It is well-known that proinflammatory mediators induce MDSC accumulation. However, the functions of cell death pathways in MDSC survival and the mechanism underlying regulation of cell death pathways in MDSCs are still elusive. Herein, we determined that DNA methylation sustains MDSC accumulation in tumor-bearing mice since pharmacological inhibition of DNMTs with Dacitabine abolished MDSC accumulation and activated antigen-specific cytotoxic T lymphocytes in tumor-bearing mice. Decreased MDSC accumulation is correlated with increased IRF8 expression in MDSCs. However, Dacitabine also abolished CD11b+Gr1+ MDSC-like cell accumulation in IRF8 KO mice, suggesting that DNA methylation regulates MDSC accumulation at the post lineage differentiation stage. Use of cell death pathway-selective inhibitors identified necroptosis as the target of DNA methylation in MDSCs. Genome-wide DNA bisulfite sequencing revealed that the promoter of Tnf is hypermethylated in tumor-induced MDSCs. Consequently, decitabine dramatically increased TNF level in MDSCs and neutralizing TNF significantly decreased Dacitabine-induced MDSC cell death. Recombinant TNF induced MDSC cell cells in a dose and RIP1-dependent manner. Inhibition of RIP1 or RIP3 did not decrease TNF expression in MDSCs. Our data determined that the TNF-RIP1 necroptosis pathway is responsible at least in part for MDSC accumulation and that the IL6-activated DNMTs hypermethylate Tnf to impair necroptosis pathway to maintain MDSC accumulation in cancer. Our data depict the IL6-STAT3-DNMT-TNFa-RIP1 necroptosis pathway as a molecular target for suppressing MDSC accumulation in cancer immunotherapy.

2020-08-01 | GSE144649 | GEO

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