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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE244130 | GEO | 2025/03/29

REPOSITORIES: GEO

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

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

2025-03-29 | GSE244129 | GEO

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: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 [RNA-seq]

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

| PRJNA1021487 | ENA

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

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.

| S-EPMC8909048 | biostudies-literature

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

2007-09-01 | E-GEOD-1925 | biostudies-arrayexpress

Cross talk between glucose metabolism and immunosuppression in IFN-γ–primed mesenchymal stem cells

Project description:This study reveals a novel relationship between mesenchymal stem cell immunomodulation and metabolism and provides a new strategy to improve their therapeutic efficacy in inflammatory diseases. The immunosuppressive function “licensed” by IFN-γ is a vital attribute of mesenchymal stem cells (MSCs) widely used in the treatment of inflammatory diseases. However, the mechanism and impact of metabolic reprogramming on MSC immunomodulatory plasticity remain unclear. Here, we explored the mechanism by which glucose metabolism affects the immunomodulatory reprogramming of MSCs “licensed” by IFN-γ. Our data showed that glucose metabolism regulates the immunosuppressive function of human umbilical cord MSCs (hUC-MSCs) challenged by IFN-γ through the Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway. Furthermore, ATP facilitated the cross talk between glucose metabolism and the JAK-STAT system, which stimulates the phosphorylation of JAK2 and STATs, as well as the expression of indoleamine 2, 3-dioxygenase and programmed cell death-1 ligand. Moreover, ATP synergistically enhanced the therapeutic efficacy of IFN-γ–primed hUC-MSCs against acute pneumonia in mice. These results indicate a novel cross talk between the immunosuppressive function, glucose metabolism, and mitochondrial oxidation and provide a novel targeting strategy to enhance the therapeutic efficacies of hUC-MSCs.

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Extracellular vesicles from IFN-γ-primed mesenchymal stem cells repress atopic dermatitis in mice.

Project description:Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by immune dysregulation, pruritus, and abnormal epidermal barrier function. Compared with conventional mesenchymal stem cell (MSC), induced pluripotent stem cell (iPSC)-derived mesenchymal stem cell (iMSC) is recognized as a unique source for producing extracellular vesicles (EVs) because it can be obtained in a scalable manner with an enhanced homogeneity. Stimulation of iMSCs with inflammatory cytokines can improve the immune-regulatory, anti-inflammatory, and tissue-repairing potential of iMSC-derived EVs. Proteome analysis showed that IFN-γ-iMSC-EVs are enriched with protein sets that are involved in regulating interferon responses and inflammatory pathways. In AD mice, expression of interleukin receptors for Th2 cytokines (IL-4Rα/13Rα1/31Rα) and activation of their corresponding intracellular signaling molecules was reduced. IFN-γ-iMSC-EVs decreased itching, which was supported by reduced inflammatory cell infiltration and mast cells in AD mouse skin; reduced IgE receptor expression and thymic stromal lymphopoietin and NF-kB activation; and recovered impaired skin barrier, as evidenced by upregulation of key genes of epidermal differentiation and lipid synthesis. IFN-γ-iMSC-EVs inhibit Th2-induced immune responses, suppress inflammation, and facilitate skin barrier restoration, contributing to AD improvement.

| S-EPMC9741801 | biostudies-literature

JAK inhibition selectively suppresses melanoma lacking IFN-γ pathway

Project description:Immune checkpoint blockers (ICBs) showed unprecedented clinical benefits. But the overall efficacy of ICBs is limited to a small subset of cancer patients due to therapeutic resistance. Concerted efforts from our group and others have identified that loss of IFN-g signaling genes in melanoma is a major mechanism of resistance to ICBs. We therefore generated B16 melanoma model with IFNgR1 knocked out by CRISPR-Cas9. We sequenced the whole transcriptomes and identified activated PI3K-Akt-mTOR pathway in IFNgR1 knocked out cells. This may represent an attractive target for therapeutic interventions to bypassing ICB resistance in melanoma lacking functional IFN-g signaling.

2022-07-31 | GSE201078 | GEO

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