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ChIP sequencing of IL-17A and IL-17F producing cells

ABSTRACT: ChIP sequencing of IL-17A and IL-17F producing cells

PROVIDER: PRJNA782123 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16991017.fastq.gz	Fastqsanger.gz
	SRR16991018.fastq.gz	Fastqsanger.gz
	SRR16991019.fastq.gz	Fastqsanger.gz
	SRR16991020.fastq.gz	Fastqsanger.gz
	SRR16991021.fastq.gz	Fastqsanger.gz

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ChIP sequencing of IL-17A and IL-17F producing cells

Project description:IL-17A has emerged as a pivotal driver of tissue pathology in many immune-mediated inflammatory diseases. Despite sharing 50% sequence homology and the same signalling pathway, the role of IL-17F remains less clear. ChIP sequencing of human IL-17 popualtions isolated using a cytokine capture technique identified clear epigenetic differences in IL-17A and IL-17F producing cells.

2023-11-20 | GSE189231 | GEO

RNA sequencing of IL-17A and IL-17F producing cells

Project description:IL-17A has emerged as a pivotal driver of tissue pathology in many immune-mediated inflammatory diseases. Despite sharing 50% sequence homology and the same signalling pathway, the role of IL-17F remains less clear. RNA sequencing of human IL-17 popualtions isolated using a cytokine capture technique identified clear transcriptional differences in IL-17A and IL-17F producing cells, with IL-17A producing cells showing enrichment for cytokine signaling and IL-17F producing cells showing enrichment for cellular replication.

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IL-17A and IL-17F producing cells

Project description:IL-17A and IL-17F producing cells

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RNA sequencing of IL-17A and IL-17F producing cells

Project description:RNA sequencing of IL-17A and IL-17F producing cells

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4-week mouse comparative study on effect of neutralizing IL-17A, IL-17F and TNFa antibodies

Project description:Molecular profiling of effect of TNFÎ± neutralization in contrast to anti-IL-17A or anti-IL-17F treatment for 28 days in lungs of M. tuberculosis infected C57BL/6 mice. Animals were treated once per week (starting day-1) with anti-mouse IL-17A or IL-17F antibodies (20 mg/kg i.p.), anti-mouse TNFÎ± antibody (10 mg/kg), respective isotype control antibodies. Moreover, infected and non-infected TNFÎ±-deficient mice were also analysed. Gene expression data revealed major changes of inflammatory and immune gene expression signatures 4 weeks post-infection (including host-pathogen interactions, macrophage recruitment, activation and polarization, host-anti-mycobacterial activities, immunomodulatory responses and extracellular matrix metallopeptidases) after TNFÎ± blockade, while IL-17A or IL-17F neutralization elicited only mild changes of few genes without impaired host resistance four weeks after M. tuberculosis infection.

2016-12-02 | E-MTAB-5218 | biostudies-arrayexpress

The expression profiles of extracellular matrix-related genes in the presence or absence of IL-17A or -17F as measured with the PCR array in systemic sclerosis (SSc) dermal fibroblasts

Project description:We examined the effect of IL-17 signaling pathway on extracellular matrix (ECM) expression and the involvement of IL-17 signaling pathway in pathogenesis of SSc. To identify differences in the expression pattern of ECM genes in IL-17A- or IL-17F-treated cells, we performed PCR array analysis, consisting of 84 ECM-related genes. Normal human dermal fibroblasts were cultured until they were confluent, and then stimulated with IL-17A or IL-17F for 12 hours, and total RNA was extracted. A mixture of equal amounts of mRNAs from three normal fibroblasts was prepared in the presence or absence of IL-17A or -17F, and mRNA expression profile was evaluated using PCR Array. Normal fibroblasts were obtained by skin biopsies from 3 healthy donors. Fibroblasts from donors were used and treated separately as indicated in the summary. Equal amount total RNA from each donor was pooled prior to gene expression analysis.

2012-01-01 | E-GEOD-33581 | biostudies-arrayexpress

The expression profiles of extracellular matrix-related genes in the presence or absence of IL-17A or -17F as measured with the PCR array in systemic sclerosis (SSc) dermal fibroblasts

2012-01-01 | GSE33581 | GEO

IL-17A-producing MAIT cells and epidermolyis bullosa inflammation

Project description:Background: Recessive Dystrophic Epidermolysis Bullosa (RDEB) is characterized by wounds chronically colonized with Staphylococcus aureus associated with local and systemic inflammation. This study aimed to clarify how the immune response is shaped by S. aureus in RDEB patients with focus on Mucosal-Associated invariant T (MAIT) cells. Methods: Fifteen RDEB children (moderate phenotype n=5; severe phenotype n=10) and controls (n=18) were enrolled. A novel proteomic pipeline was used to evaluate over 800 proteins in plasma. Patient-specific cytokine, immune T cell and S. aureus signatures were evaluated. The effect of the patient's S. aureus strain on T-cell function was analyzed in vitro and correlated with the bacterial secretome. Findings: We detected a unique plasma proteomic signature that enabled the differentiation of RDEB children and controls. Profiling of immune cells (n= 30 subsets and cytokine-producing cells) and cytokines (n=38) identified a severe inflammatory response and activation of CD4+ T and MAIT cells in severe RDEB patients with increased frequency of IL-17A-producing CD4+ T and MAIT cells. Positive S. aureus cultures from the skin of 12 of the 15 RDEB patients allowed whole-genome sequencing of patient strains, assessment of the primary keratinocyte response to bacterial challenge, and identification of potential immunomodulatory bacterial determinants. Conditioned media from keratinocytes challenged with S. aureus strains of severe RDEB patients induced a strong Th17 response. Interpretation: This study uncovers a huge systemic inflammatory response associated with a high level of circulating IL-17A-producing CD4+ T and MAIT cells in RDEB patients and supports the involvement of patient S. aureus strains in biasing the host immune response.

2025-07-21 | PXD049374 | Pride

Corral2021 - Interplay between SMAD2 and STAT5A regulating IL-17A/F expression in Th cells.

Project description:IL-17A and F are critical cytokines in anti-microbial immunity but also contribute to auto-immune pathologies. Recent evidence suggests that they may be differentially produced by T-helper (Th) cells but the underlying mechanisms remain unknown. To address this question, a logical model containing 82 components and 136 regulatory links was developed and calibrated with original flow cytometry data using naive CD4+ T cells in conditions inducing either IL-17A or F. Model analyses led to the identification of the transcription factors NFAT2A, STAT5A and Smad2 as key components explaining the differential expression of IL-17A and IL-17F, with STAT5A controlling IL-17F expression, and an interplay of NFAT2A, STAT5A and Smad2 controlling IL-17A expression.

2021-04-06 | MODEL2101150001 | BioModels

CD4+ tissue resident memory Th17 cells drive IL-17A-mediated joint pathology in Spondyloarthritis

Project description:Interleukin (IL)-17A plays a central role in driving joint pathology in Spondyloarthritis (SpA). In this study, synovial tissues from patients with Axial SpA and Psoriatic arthritis were analyzed using single-cell RNA sequencing and spatial RNA profiling to pinpoint the cellular source of IL-17A. The results revealed that IL-17A expression is exclusively localized to CD4⁺CXCR6⁺ tissue resident memory Th17 (TRM17) cells, which interact with activated CLEC10A⁺ dendritic cells within the joint. These interactions coincide with an enhanced IL-17A response signature in both sublining and lining fibroblasts. Furthermore, in vitro-generated TRM17-like cells from blood memory CD4⁺ T cells recapitulated the in situ characteristics by producing IL-17A in response to T cell receptor stimulation, while IL-23 selectively amplified TCR-mediated IL-17F and IFN-γ production. Importantly, perturbation of the epigenetic regulator BRD1 impaired the generation of TRM17-like cells. These findings underscore the predominant role of TRM17 cells as the source of IL-17A in SpA and suggest that targeting BRD1 or depleting TRM17 cells may offer promising therapeutic strategies for achieving long-term disease remission.

2025-05-29 | GSE290921 | GEO

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