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Type I Interferon Response in Astrocytes Promotes Brain Metastasis by Enhancing Monocytic Myeloid Cell Recruitment

ABSTRACT: Type I Interferon Response in Astrocytes Promotes Brain Metastasis by Enhancing Monocytic Myeloid Cell Recruitment

PROVIDER: PRJNA930486 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23310592.fastq.gz	Fastqsanger.gz
	SRR23310593.fastq.gz	Fastqsanger.gz
	SRR23310594.fastq.gz	Fastqsanger.gz
	SRR23310595.fastq.gz	Fastqsanger.gz
	SRR23310596.fastq.gz	Fastqsanger.gz

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Type I Interferon Response in Astrocytes Promotes Brain Metastasis by Enhancing Monocytic Myeloid Cell Recruitment

Project description:Cancer metastasis to the brain is a significant clinical problem. Metastasis is the consequence of favorable interactions between invaded cancer cells and the microenvironment. Here, we demonstrate that cancer-activated astrocytes create a sustained low-level activated type I interferon (IFN) microenvironment in brain metastatic lesions. We further confirm that the IFN response in astrocytes facilitate brain metastasis. Mechanistically, IFN signaling in astrocytes activates C-C Motif Chemokine Ligand 2 (CCL2) production, which further increases the recruitment of monocytic myeloid cells. The correlation between CCL2 and monocytic myeloid cells is confirmed in clinical brain metastasis samples. Lastly, genetically or pharmacologically inhibiting C-C Motif Chemokine Receptor 2 (CCR2) significantly reduces brain metastases. Our study clarifies a pro-metastatic effect of type I IFN in the brain even though IFN response has been considered to have anti-tumor effects. Moreover, this work expands our understandings on the interactions between cancer-activated astrocytes and immune cells in brain metastasis.

2023-03-16 | GSE224302 | GEO

Type I interferon response in astrocytes promotes brain metastasis by enhancing monocytic myeloid cell recruitment.

Project description:Cancer metastasis to the brain is a significant clinical problem. Metastasis is the consequence of favorable interactions between invaded cancer cells and the microenvironment. Here, we demonstrate that cancer-activated astrocytes create a sustained low-level activated type I interferon (IFN) microenvironment in brain metastatic lesions. We further confirm that the IFN response in astrocytes facilitates brain metastasis. Mechanistically, IFN signaling in astrocytes activates C-C Motif Chemokine Ligand 2 (CCL2) production, which further increases the recruitment of monocytic myeloid cells. The correlation between CCL2 and monocytic myeloid cells is confirmed in clinical brain metastasis samples. Lastly, genetically or pharmacologically inhibiting C-C Motif Chemokine Receptor 2 (CCR2) reduces brain metastases. Our study clarifies a pro-metastatic effect of type I IFN in the brain even though IFN response has been considered to have anti-tumor effects. Moreover, this work expands our understandings on the interactions between cancer-activated astrocytes and immune cells in brain metastasis.

| S-EPMC10163863 | biostudies-literature

Proteomic profiling of interferon-responsive reactive astrocytes in rodent and human

Project description:Astrocytes are a heterogenous population of glial cells that respond to pathological insults or injury by undergoing a profound transformation called reactivity. Reactive astrocytes exhibit distinct, context-dependent cellular, molecular, and functional states that can either help or hinder tissue homeostasis. We recently identified a subtype of reactive astrocytes in the mouse brain called interferon-responsive reactive astrocytes (IRRAs), defined by interferon-responsive genes like Igtp, Ifit3, Oasl, Mx1, Cxcl10, and Gbp2 . To further this transcriptomic definition of IRRAs, we wanted to define the proteomic changes that occur in this sub-state.

2023-03-07 | MSV000091426 | MassIVE

SETDB1 suppresses interferon responses and NK cell-mediated immunosurveillance specifically in monocytic AML: CRISPR/Cas9 screens on cSAM leukemia cells

Project description:Monocytic acute myeloid leukemia (AML) responds poorly to current treatments, including venetoclax-based therapy. We conducted in vivo and in vitro CRISPR/Cas9 library screenings using a mouse monocytic AML model, and identified SETDB1 and its binding partners (ATF7IP and TRIM33) as crucial tumor promoters in vivo. The growth-inhibitory effect of Setdb1 depletion in vivo was mainly dependent on NK cell-mediated cytotoxicity. Mechanistically, SETDB1 depletion upregulated interferon-stimulated genes and NKG2D ligands through demethylation of histone H3 Lys9 at the monocyte-specific enhancer regions, thereby enhancing their immunogenicity to NK cells and intrinsic apoptosis. Importantly, these effects were not observed in non-monocytic leukemia cells. We also identified the expression of MNDA and its murine counterpart Ifi203 as biomarkers to predict the sensitivity of each AML to SETDB1 depletion. Our study highlights the critical and selective role of SETDB1 in monocytic AML and underscores its potential as a therapeutic target for current unmet needs.

2024-08-03 | GSE270630 | GEO

SETDB1 suppresses interferon responses and NK cell-mediated immunosurveillance specifically in monocytic AML: H3K9me3 ChIP-seq of cSAM leukemia cells with Setdb1 depletion [ChIP-seq]

2024-08-03 | GSE266098 | GEO

SETDB1 suppresses interferon responses and NK cell-mediated immunosurveillance specifically in monocytic AML: Gene expression profiles of cSAM leukemia cells with Setdb1 depletion [RNA-seq]

2024-08-03 | GSE266097 | GEO

BPIFA1 Regulates Interferon-Mediated Lung Neutrophil Recruitment During Acute Inflammation

Project description:BPIFA1 Regulates Interferon-Mediated Lung Neutrophil Recruitment During Acute Inflammation

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The transcriptome of type I murine astrocytes under interferon-gamma exposure and remyelination stimulus

Project description:Astrocytes are considered as an important contributor of the central nervous system (CNS) disorders, and particularly multiple sclerosis. Transcriptome of these cells is greatly affected by cytokines released by lymphocytes penetrating the blood-brain barrier, particularly classical pro-inflammatory cytokine interferon-gamma (IFN-gamma). We report here transcriptomal profiling of astrocytes treated by IFN-gamma and perspective remyelinization agent benztropine. Our findings indicate that expression of genes involved in antigen processing and presentation in astrocytes are significantly upregulated upon IFN-gamma exposure emphasizing critical role of this cytokine in redirecting of immune response towards self-antigens. Data reported herein support previous observations that IFN-gamma-induced JAK-STAT signaling pathway may be regarded as valuable target for the pharmaceutical intervention.

2017-03-23 | GSE96899 | GEO

Enhancing GAT-3 in thalamic astrocytes promotes resilience to brain injury in rodents

Project description:Enhancing GAT-3 in thalamic astrocytes promotes resilience to brain injury in rodents

| PRJNA838581 | ENA

Interferon-alpha mediates the development of autoimmunity by direct tissue toxicity and through immune-cell recruitment mechanisms

Project description:Interferon-alpha is a major therapeutic agent for many diverse diseases. However, the interferon-alpha mechanism of therapeutic action and associated side effects are not well understood. In particular, thyroiditis is a common unexplained complication. We hypothesized that direct thyroid-toxic actions coupled with immune mechanisms play a major role in the thyroiditis etiology. To test this hypothesis, we investigated the actions of interferon-alpha on cultured thyrocytes in vitro, and in vivo by creating transgenic mice overexpressing interferon-alpha tissue specifically in thyrocytes. Interferon-alpha treatment of cultured PCCL3 rat thyrocytes increased markers of thyroid differentiation, levels of MHC class I, and expression of heat shock protein and CXCL10. This was associated with markedly increased nonapoptotic thyroid cell death. Consistent with these in vitro findings, transgenic mice overexpressing interferon-alpha in the thyroid displayed striking thyroid cell death characteristic of nonimmune thyroid destruction that progressed to profound primary hypothyroidism. Moreover, genes linked to cell death pathways, granzyme B, or known to be associated with recruitment of a cytotoxic immune response, CXCL10, interleukin-23, and TRIM21 were increased in the transgenic thyroids. Taken together, the etiology of interferon-induced thyroiditis likely involves both a direct toxic action on thyrocytes, as well as provocation of a destructive immune response. 1) Thyroid cells were incubated with interferon-alpha, and global gene expression was determined by RNA-seq. 2) Thyroid tissues were obtained from transgenic mice overexpressing interferon-alpha and from wild type mice, and global gene expression was analyzed using RNA-seq.

2011-11-03 | E-GEOD-25115 | biostudies-arrayexpress

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