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DNA hypomethylation ameliorates erosive inflammatory arthritis by modulating interferon regulatory factor-8

ABSTRACT: DNA hypomethylation ameliorates erosive inflammatory arthritis by modulating interferon regulatory factor-8

PROVIDER: PRJNA1068034 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27697335_1.fastq.gz	Fastqsanger.gz
	SRR27697335_2.fastq.gz	Fastqsanger.gz
	SRR27697336_1.fastq.gz	Fastqsanger.gz
	SRR27697336_2.fastq.gz	Fastqsanger.gz
	SRR27697337_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

DNA hypomethylation ameliorates erosive inflammatory arthritis by modulating interferon regulatory factor-8

2024-01-23 | GSE253974 | GEO

DNA hypomethylation ameliorates erosive inflammatory arthritis by modulating interferon regulatory factor-8.

Project description:Epigenetic regulation plays a crucial role in the pathogenesis of autoimmune diseases such as inflammatory arthritis. DNA hypomethylating agents, such as decitabine (DAC), have been shown to dampen inflammation and restore immune homeostasis. In the present study, we demonstrate that DAC elicits potent anti-inflammatory effects and attenuates disease symptoms in several animal models of arthritis. Transcriptomic and epigenomic profiling show that DAC-mediated hypomethylation regulates a wide range of cell types in arthritis, altering the differentiation trajectories of anti-inflammatory macrophage populations, regulatory T cells, and tissue-protective synovial fibroblasts (SFs). Mechanistically, DAC-mediated demethylation of intragenic 5'-Cytosine phosphate Guanine-3' (CpG) islands of the transcription factor Irf8 (interferon regulatory factor 8) induced its re-expression and promoted its repressor activity. As a result, DAC restored joint homeostasis by resetting the transcriptomic signature of negative regulators of inflammation in synovial macrophages (MerTK, Trem2, and Cx3cr1), TREGs (Foxp3), and SFs (Pdpn and Fapα). In conclusion, we found that Irf8 is necessary for the inhibitory effect of DAC in murine arthritis and that direct expression of Irf8 is sufficient to significantly mitigate arthritis.

| S-EPMC10873594 | biostudies-literature

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

Osteoclast microRNA profiling to capture the erosive factor in rheumatoid arthritis

Project description:Background: In rheumatoid arthritis (RA), only a subset of patients develop an irreversible bone destruction. Our aim was to develop a microRNA (miR)-based osteoclast-related signature to predict erosiveness in RA. Results: We identified 5 miRs from PBMC-derived osteoclasts differentially expressed in RNASeq also in qPCR assessment. Conclusion: We found 5 miRNAs differentially refulated in erosive rheumtoid arhtritis compare to no erosve patient. This study could improve the current approach to identify RA subjects at risk of erosions, by adding biomarker signatures based on the profile of miRs in the osteoclasts.

2023-09-01 | GSE209982 | GEO

Osteoclast microRNA profiling to capture the erosive factor in rheumatoid arthritis

Project description:Osteoclast microRNA profiling to capture the erosive factor in rheumatoid arthritis

| PRJNA863270 | ENA

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

SIRPa agonist antibody treatment ameliorates experimental arthritis and colitis

Project description:SIRPa agonist antibody treatment ameliorates experimental arthritis and colitis

| PRJNA993132 | ENA

Transcriptomic characterization of classical monocytes highlights the involvement of immuno-inflammation in bone erosion in Rheumatoid Arthritis

Project description:Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with localized bone involvement characterized by the presence of bone erosions. Evidence-based data suggest that under inflammatory conditions, classical monocytes are the main source of osteoclasts and might be involved in bone erosion pathophysiology. Here, we analyze the transcriptomic profile of classical monocytes in erosive and non-erosive rheumatoid arthritis patients in order to better understand their contribution to bone erosion. Thirty-nine premenopausal RA patients and 20 healthy age-matched women were recruited for this study. Classical monocytes were isolated from peripheral blood through negative selection. Sequencing library was constructed using the Quant-seq® 30 mRNA-Seq Library Prep Kit (Lexogen®) and sequenced using an Illumina Seq 2500 platform (Illumina®). Differential expression analysis was performed between patients and control groups. Therefore, gene sets analysis was performed to identify the enriched biological pathways. Results suggested that alterations in pathways related to the inflammatory process and impairment of bone formation have an important role in the pathophysiology of bone erosions in patients with rheumatoid arthritis.

2023-09-19 | E-MTAB-13361 | biostudies-arrayexpress

SIRPa agonist antibody treatment ameliorates experimental arthritis and colitis [array]

Project description:The innate immune system is finely tuned to enable. rapid response to pathogenic stimuli but keep quiescent during tissue homeostasis. Balance of activating and inhibitory signaling sets a threshold for immune activation. Signal regulatory protein (SIRPa) is an immune inhibitory receptor expressed by myeloid cells and interacts with CD47 to inhibit immune cell phagocytosis, migration, and activation. Despite the progress of SIRPa and CD47 antagonist antibodies to promote anti-cancer immunity, it is not yet known whether therapeutic SIRPa receptor agonism could restrain excessive autoimmune inflammation in the context of autoimmunity. Here, we reported that increased neutrophil- and monocyte-associated genes including SIRPA in inflamed tissues biopsies of rheumatoid arthritis and inflammatory bowel diseases, and elevated SIRPA in colonic biopsies is associated with treatment refractory ulcerative colitis patients. We next identified a novel agonistic anti-SIRPa antibody that exhibited potent anti-inflammatory effects in reducing neutrophil and monocytes chemotaxis and tissue infiltration. In preclinical models of arthritis and colitis, anti-SIRPa agonistic antibody ameliorates autoimmune joint inflammation and inflammatory colitis through reducing neutrophils and monocytes in tissues. Our work provides a proof-of-concept for SIRPa receptor agonism for suppressing excessive innate immune activation and autoimmune inflammatory therapeutic treatment

2023-08-24 | GSE236924 | GEO

SIRPa agonist antibody treatment ameliorates experimental arthritis and colitis [sequencing]

Project description:The innate immune system is finely tuned to enable rapid response to pathogenic stimuli but keep quiescent during tissue homeostasis.Balance of activating and inhibitory signaling sets a threshold for immune activation. Signal regulatory protein (SIRPa) is an immune inhibitory receptor expressed by myeloid cells and interacts with CD47 to inhibit immune cell phagocytosis, migration, and activation. Despite the progress of SIRPa and CD47 antagonist antibodies to promote anti-cancer immunity, it is not yet known whether therapeutic SIRPa receptor agonism could restrain excessive autoimmune inflammation in the context of autoimmunity. Here, we reported that increased neutrophil- and monocyte-associated genes including SIRPA in inflamed tissues biopsies of rheumatoid arthritis and inflammatory bowel diseases, and elevated SIRPA in colonic biopsies is associated with treatment refractory ulcerative colitis patients. We next identified a novel agonistic anti-SIRPa antibody that exhibited potent anti-inflammatory effects in reducing neutrophil and monocytes chemotaxis and tissue infiltration. In preclinical models of arthritis and colitis, anti-SIRPa agonistic antibody ameliorates autoimmune joint inflammation and inflammatory colitis through reducing neutrophils and monocytes in tissues. Our work provides a proof-of-concept for SIRPa receptor agonism for suppressing excessive innate immune activation and autoimmune inflammatory therapeutic treatment

2023-08-24 | GSE235400 | GEO

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