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Transcriptional response of human synovial fibroblasts to TNF and IL-17A (Microarray Data 2)

ABSTRACT: Transcriptional response of human synovial fibroblasts to TNF and IL-17A (Microarray Data 2)

PROVIDER: PRJNA531480 | ENA |

REPOSITORIES: ENA

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Transcriptional response of human synovial fibroblasts to TNF and IL-17A (Microarray Data 2)

Project description:The combination of TNF and IL-17A has synergistic effects on the transcription of genes encoding chemokines and cytokines.

2017-01-18 | GSE93720 | GEO

Transcriptional response of human synovial fibroblasts to TNF and IL-17A over time (Microarray Data 1)

Project description:The combination of TNF and IL-17A has synergistic effects on the transcription of genes encoding chemokines and cytokines.

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Transcriptional response of human synovial fibroblasts to TNF and IL-17A

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Gene Expression Profiling of IL-17A-treated Synovial Fibroblasts from the Human Temporomandibular Joint

Project description:Synovial fibroblasts contribute to the inflammatory temporomandibular joint under pathogenic stimuli. Synovial fibroblasts and T cells participate in the perpetuation of joint inflammation in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. IL-17 is an inflammatory cytokine produced primarily by Th17 cells that plays critical roles in the pathogenesis of numerous autoimmune and inflammatory diseases. Here, we investigated the roles of IL-17A in temporomandibular joint disorders (TMD) by using genome-wide analysis of synovial fibroblasts isolated from patients with TMD. We analyzed the gene expression profiles of synovial fibroblasts that were treated with or without IL-17A. IL-17 induced gene expression in synovial fibroblasts from human temporomandibular joint was measured at 4 hours after treated with IL-17A (10 ng/ml) and untreated control samples. This experiment used one donor sample.

2015-11-05 | E-GEOD-74668 | biostudies-arrayexpress

Transcriptional responses of human synovial fibroblasts to TNF and IL-17A over time (RNA-seq Data 1)

Project description:The combination of TNF and IL-17A has synergistic effects on the transcription of genes encoding chemokines and cytokines.

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Gene Expression Profiling of IL-17A-treated Synovial Fibroblasts from the Human Temporomandibular Joint

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RNA-seq analysis of IL-17A+/IFNy+ CD8+ and IL-17A+CD4+ T cells from Psoriatic Arthritis Synovial Fluid

Project description:Psoriatic arthritis is a seronegative polyarticular form of inflammatory arthritis . Genetic analysis implicates a role for both IL-17/23 axis and CD8+ T cells in disease susceptibility. Using RNA-seq we identified differential gene expression between synovial IL-17A+(IFNy+/-) CD8+ T cells compared to IL-17A-IFNy+ CD8+ T cells and IL-17A+CD4+ T cells from the synovial fluid of psoriatic arthritis patients. We find that IL-17A+CD8+ T cells have a transcriptional overlap with IL-17A+CD4+ T cells. Overall we show these IL-17A+ CD8+ T cells have a polyfunctional, pro-inflammatory capacity and are potentially derived from common precursors, shared with IL-17A-CD8+ T cells.

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Effects of siRNA gene silencing on transcriptional responses of human synovial fibroblasts to TNF and IL-17A (RNA-seq Data 2)

Project description:TNF and IL-17A synergistic effects on gene expression after silencing CUX1, LIFR, STAT3, STAT4, ELF3

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Transcriptional response of human synovial fibroblasts to TNF and IL-17A over time (Microarray Data 1)

Project description:Transcriptional response of human synovial fibroblasts to TNF and IL-17A over time (Microarray Data 1)

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Interleukin-17A causes osteoarthritis-like transcriptional changes in human osteoarthritis-derived chondrocytes and synovial fibroblasts in vitro

Project description:Increased interleukin (IL)-17A has been identified in joints affected by osteoarthritis (OA), but it is unclear how IL-17A, and its family members IL-17AF and IL-17F, can contribute to human OA pathophysiology. Therefore, we aimed to evaluate the gene expression and signalling pathway activation effects of the different IL-17 family members in chondrocytes and fibroblasts derived from cartilage and synovium of patients with end-stage knee OA. Chondrocytes and synovial fibroblasts derived from end-stage OA patients were treated with IL-17A, IL-17AF, or IL-17F, and gene expression was assessed with bulk RNA-Seq. Hallmark pathway analysis showed that IL-17 cytokines regulated several OA pathophysiology-related pathways including immune-, angiogenesis-, and complement-pathways in both chondrocytes and synovial fibroblasts derived from end-stage OA patients. While overall IL-17A induced the strongest transcriptional response, followed by IL-17AF and IL-17F, not all genes followed this pattern. Disease-Gene Network analysis revealed that IL-17A-related changes in gene expression in these cells are associated with experimental arthritis, knee arthritis, and musculoskeletal disease gene-sets. In conclusion, the association of IL-17-induced transcriptional changes with arthritic gene-sets supports a role for IL-17A in OA pathophysiology.

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