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Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages [RNA-seq]

ABSTRACT: We analyzed mRNA sequences to demonstrate selective regulation of genetic programs by JAKi in IFN-γ primed human macrophages.

ORGANISM(S): Homo sapiens

PROVIDER: GSE244129 | GEO | 2025/03/29

REPOSITORIES: GEO

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Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages [ATAC-seq]

Project description:We analyzed ATAC sequences to demonstrate selective regulation of genetic programs by JAKi in IFN-γ primed human macrophages.

2025-03-29 | GSE244128 | GEO

Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-03-29 | GSE244130 | GEO

Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages

Project description:Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages

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Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages [ATAC-seq]

Project description:Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages [ATAC-seq]

| PRJNA1021486 | ENA

Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages [RNA-seq]

Project description:Epigenomic Landscapes Define Differential JAK Inhibitor Sensitivity in IFN-γ-Primed Human Macrophages [RNA-seq]

| PRJNA1021487 | ENA

Transcription profiling of IFN-gamma transcriptional responses in control and IFN-gamma primed primary human macrophages

Project description:IFN-gamma transcriptional responses in control and IFN-gamma primed primary human macrophages

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IFN-γ Induces PD-L1 Expression in Primed Human Basophils.

Project description:Programmed death-ligand 1 (PD-L1) plays a key role in maintaining immune tolerance and also in immune evasion of cancers and pathogens. Though the identity of stimuli that induce PD-L1 in various human innate cells and their function are relatively well studied, data on the basophils remain scarce. In this study, we have identified one of the factors, such as IFN-γ, that induces PD-L1 expression in human basophils. Interestingly, we found that basophil priming by IL-3 is indispensable for IFN-γ-induced PD-L1 expression in human basophils. However, priming by other cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF) and thymic stromal lymphopoietin (TSLP) was dispensable. Analyses of a published microarray data set on IL-3-treated basophils indicated that IL-3 enhances IFNGR2, one of the chains of the IFNGR heterodimer complex, and CD274, thus providing a mechanistic insight into the role of IL-3 priming in IFN-γ-induced PD-L1 expression in human basophils.

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Analyzing small RNA sequences from canine stem cell-derived extracellular vesicles primed with TNF-α and IFN-γ

Project description:Acute lung injury is an acute inflammation disorder that disrupts the lung endothelial and epithelial barriers. In this study, we investigated the extracellular vesicles (EVs) obtained via priming inflammatory cytokines such as tumor necrosis factor (TNF)-α and interferon (IFN)-γ on canine adipose mesenchymal stem cells in improving their anti-inflammatory and/or immunosuppressive potential, and/or their ability to alleviate lipopolysaccharide-induced lung injury in vitro. We also explored the correlation between epithelial-to-mesenchymal transition and the inflammatory repressive effect of primed EVs. Using small RNA-Seq, we confirmed that miR-16 and miR-502 significantly increased in EVs from TNF-α and IFN-γ-primed canine adipose mesenchymal stem cells. The pro and anti-inflammatory cytokines were analyzed in a lipopolysaccharide-induced lung injury model and we found that the EV anti-inflammatory effect improved on priming with inflammatory cytokines. EVs obtained from primed stem cells effectively suppress endothelial-to-mesenchymal transition in a lung injury model. Our results suggest a potential therapeutic approach utilizing EVs obtained from adipose mesenchymal stem cells primed with TNF-α and IFN-γ against lung inflammation and endothelial to mesenchymal transition.

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RNA-seq of C3H/HeJ AA mice skin biopsies treated with JAK-selective inhibitors

Project description:To define the molecular response to JAKi treatment, we performed RNA-seq analysis on a series of skin biopsies taken before and after systemic treatment with INCB039110 (JAK1i), CEP-33779 (JAK2i), PF-06651600 (JAK3i), ruxolitinib (JAK1/2i), tofacitinib (pan-JAKi) or vehicle control.

2021-02-24 | GSE167360 | GEO

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