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Cish attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function

ABSTRACT: Cish attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function

PROVIDER: PRJNA659673 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12532525_1.fastq.gz	Fastqsanger.gz
	SRR12532525_2.fastq.gz	Fastqsanger.gz
	SRR12532526_1.fastq.gz	Fastqsanger.gz
	SRR12532526_2.fastq.gz	Fastqsanger.gz
	SRR12532527_1.fastq.gz	Fastqsanger.gz

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Cish attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function

Project description:Lung-specific expression of the SOCS family member Cish is driven by steady-state GM-CSF signaling and shapes alveolar macrophage identity and homeostatic function.

2021-08-26 | GSE156967 | GEO

CISH attenuates homeostatic cytokine signaling to promote lung-specific macrophage programming and function.

Project description:Tissue-specific cytokine stimuli orchestrate specialized homeostatic functions of resident macrophages. In the lung, steady-state signaling by the cytokine GM-CSF is critical for alveolar macrophage (AM) development and function. Here, we showed that CISH, a suppressor of cytokine signaling (SOCS) family member that is acutely induced by diverse cytokine stimuli in many tissues, was expressed constitutively in AMs in response to steady-state GM-CSF signaling. Cish deficiency led to the generation of foamy AMs and the accumulation of pulmonary surfactant. These phenotypic changes were associated with enhanced activation of STAT5, AKT, and ERK and increased expression of the gene encoding the transcription factor GATA2. RNA-seq analysis of Cish−/− AMs revealed a set of dysregulated immune and lipid-process modules, including the increased expression of genes enriched for GATA2-binding motifs. Last, Cish-deficient, bone marrow–derived macrophages showed increased Gata2 expression and accumulated more lipid upon incubation with bronchoalveolar lavage fluid compared with Cish-sufficient cells. Thus, CISH is part of a feedback loop that constrains homeostatic cytokine signaling and Gata2 expression to maintain AM identity and function.

| S-EPMC8982672 | biostudies-literature

Cish inhibits CD8+ T cell immunity and disrupts proximal T cell receptor signaling

Project description:T cell receptor (TCR) signaling is a critical process in immunity to infectious disease and cancer. Recently, a genome-wide association study has implicated polymorphisms in the CISH locus with susceptibility to infectious diseases. However, the role of Cish in the immune responses and its molecular underpinnings remains unclear. Here we demonstrate that Cish deletion resulted in protection against viral infection and enhanced CD8+ T cell tumor immunity. Transcriptome profiling revealed a hyper-TCR activation signature in Cish-deficient CD8+ T cells. Subsequent analysis revealed an inhibitory role for Cish in PLCγ1 activation, ensuing Ca2+ release and downstream signaling. In the steady-state Cish was found to physically interact with PLCγ1, however, PLCγ1 was only found to be ubiquitinated after acute TCR stimulation in the presence of Cish. These data implicate Cish as a potent negative regulator of TCR signaling and T cell immunity to infection and cancer and may have significant clinical applications. 4 biological replicates from wild-type mice and 3 biological replicates from Cish knock-out (-/-) mice were analyzed.

2015-04-30 | E-GEOD-56328 | biostudies-arrayexpress

Cish inhibits CD8+ T cell immunity and disrupts proximal T cell receptor signaling

2015-04-30 | GSE56328 | GEO

Quantitative Analysis of Wild Type and CISH-/- induced pluripotent stem cell derived NK cells (iPSC-NK) Transcriptomes

Project description:We developed human CISH-knockout (CISH-/-) NK cells using an induced pluripotent stem cell-derived NK cell (iPSC-NK cell) platform. And compare transcriptomes of CISH-/- iPSC NK cells with wild type iPSC NK cells using RNA seq. RNA seq data suggested that genes involved in the JAK-STAT signaling pathway and lymphocyte activations were significantly activated in CISH-/- iPSC NK cells.

2020-05-09 | GSE150155 | GEO

Psidium guajava cultivar:CISH-G5

Project description:Psidium guajava cultivar:CISH-G5 Raw sequence reads

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Epigenomic and Functional Convergence Between Glucocorticoid- and IL4-Driven Macrophage Programming

Project description:Macrophages adopt distinct phenotypes in response to environmental cues, with type-2 cytokine interleukin-4 (IL4) promoting a tissue-repair homeostatic state (M2IL4). Glucocorticoids, widely used anti-inflammatory therapeutics, reportedly impart a similar phenotype (M2GC), but how or to what extent these populations functionally converge is unknown. We show that M2IL4 and M2GC transcriptomes share a striking overlap mirrored by a shift in chromatin landscape in both common and signal-specific gene subsets. This core homeostatic program is enacted by transcriptional effectors KLF4 and the GC receptor, whose genome-wide occupancy and actions are integrated in a stimulus-specific manner by the nuclear receptor cofactor GRIP1. Indeed, many of the M2IL4:M2GC-shared transcriptomic changes were GRIP1-dependent. Consistently, GRIP1 loss attenuated phagocytic activity of both populations in vitro and macrophage tissue-repair properties in the murine colitis model in vivo. These findings provide a mechanistic framework for homeostatic macrophage programming by distinct signals, to better inform anti-inflammatory drug design.

2024-09-03 | GSE250376 | GEO

Epigenomic and Functional Convergence Between Glucocorticoid- and IL4-Driven Macrophage Programming [ATAC-seq]

Project description:Macrophages adopt distinct phenotypes in response to environmental cues, with type-2 cytokine interleukin-4 (IL4) promoting a tissue-repair homeostatic state (M2IL4). Glucocorticoids - widely used anti-inflammatory therapeutics - reportedly impart a similar phenotype (M2GC), however how or to what extent these populations functionally converge is unknown. We show that M2IL4 and M2GC transcriptomes share a striking overlap mirrored by a shift in chromatin landscape in both common and signal-specific gene subsets. This core homeostatic program is enacted by transcriptional effectors KLF4 and the GC receptor (GR), whose genome-wide occupancy and actions are integrated in a stimulus-specific manner by the nuclear receptor cofactor GRIP1. Indeed, 35% of the shared IL4- vs. GC-elicited transcriptomic changes were GRIP1-dependent. Consistently, GRIP1 loss attenuated M2IL4 and M2GC phagocytic activity in vitro and macrophage tissue-repair properties in the murine colitis model in vivo. These findings provide a mechanistic framework for homeostatic macrophage programming by distinct signals, to better inform GR-targeting drug design.

2024-09-03 | GSE248042 | GEO

Pro-inflammatory cytokine blockade attenuates myeloid expansion in a murine model of rheumatoid arthritis

Project description:Pro-inflammatory cytokine blockade attenuates myeloid expansion in a murine model of rheumatoid arthritis

| PRJNA531613 | ENA

Mangifera indica isolate:CISH BlockII | cultivar:Amrapali

Project description:Mangifera indica isolate:CISH BlockII | cultivar:Amrapali Transcriptome or Gene expression

| PRJNA313340 | ENA