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Effect of T cell supernatants or cytokines on synovial fibroblasts

ABSTRACT: Effect of T cell supernatants or cytokines on synovial fibroblasts

PROVIDER: PRJNA835731 | ENA |

REPOSITORIES: ENA

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Effect of T cell supernatants or cytokines on synovial fibroblasts

Project description:To investigate the effects of soluble factors produced by synovial CD8 T cells, we stimulated human rheumatoid arthritis (RA) synovial fibroblasts with supernatants from synovial fluid CD8 T cells, blood CD8 T cells, or synovial fluid CD4 T cells stimulated with anti-CD3/CD28 antibody-coated beads. For comparison, we stimulated RA synovial fibroblasts with recombinant TNF or interferon-gamma or T cell supernatants pre-incubated with TNF-blocking antibodies.

2022-05-08 | GSE202367 | GEO

Pro-inflammatory cytokines drive functional deregulation of potassium channels in primary synovial fibroblasts

Project description:Pro-inflammatory cytokines drive functional deregulation of potassium channels in primary synovial fibroblasts

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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.

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

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Synovial fibroblasts, RA versus OA

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Pro-inflammatory cytokines drive functional deregulation of potassium channels in primary synovial fibroblasts

Project description:The synovium secretes synovial fluid but is also richly innervated with nociceptors and acts as a gateway between avascular joint tissues and the circulatory system. Resident fibroblast-like synoviocytes’ (FLS) calcium-activated potassium channels (KCa) change in activity in arthritis models and this correlates with FLS activation. To deepen our understanding of the synovium in the context of synovial joint health and disease, the electrophysiological profile of FLS cells needs to be characterised, along with the ion channels that are present. Ion channels are an essential component of any cell membrane that controls ion movement in and out of the cell and play an important role in a multitude of cell regulating processes, typically by modulating the membrane potential To this end, we chose to perform an UNBIASED screen to identify/screen the ion channels that are transcribed in these cells and determine if this "channelome" changes with cytokine exposure. PCR/Westerns naturally bias toward the known proteins and transcripts and so we used Next Generation sequencing to scan the entire transcriptome. Objective: To determine the mechanism of this activation in an in vitro model of inflammatory arthritis; 72hr treatment with the cytokines TNFa and IL1b.

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Modulation of the TNF-induced macrophage response by synovial fibroblasts

Project description:Here we explored how the human macrophage response to tumor necrosis factor (TNF) is regulated by human synovial fibroblasts, the representative stromal cell type in the synovial lining of joints that become activated during inflammatory arthritis. Genome-wide transcriptome analysis (RNAseq) showed that co-cultured synovial fibroblasts modulate the expression of approximately one third of TNF-inducible genes in macrophages, including expression of target genes in pathways important for macrophage survival and polarization towards an alternatively activated phenotype. This work furthers our understanding of the interplay between innate immune and stromal cells during an inflammatory response, one that is particularly relevant to inflammatory arthritis. Our findings also identify modulation of macrophage phenotype as a new function for synovial fibroblasts that may prove to be a contributing factor in arthritis pathogenesis.

2014-08-04 | GSE57723 | GEO

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