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CXCL9 links skin inflammation and fibrosis via CXCR3-dependent upregulation of collagen 1a1 in fibroblasts

ABSTRACT: CXCL9 links skin inflammation and fibrosis via CXCR3-dependent upregulation of collagen 1a1 in fibroblasts

PROVIDER: PRJNA777251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16700301_1.fastq.gz	Fastqsanger.gz
	SRR16700301_2.fastq.gz	Fastqsanger.gz
	SRR16700302_1.fastq.gz	Fastqsanger.gz
	SRR16700302_2.fastq.gz	Fastqsanger.gz
	SRR16700303_1.fastq.gz	Fastqsanger.gz

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CXCL9 links skin inflammation and fibrosis via CXCR3-dependent upregulation of collagen 1a1 in fibroblasts

Project description:We performed a comparative transcriptomics study of murine immune, fibrotic and skin gene expression profiles in subcutaneous bleomycin injection to determine whether this model mirrors human morphea (localized scleroderma).

2024-10-22 | GSE187002 | GEO

Transcriptomic profiling of CXCR3+/- SUM-159-LM1 breast cancer cells

Project description:Cancer-associated fibroblasts promote the development of many primary malignancies, but their function in metastatic progression is poorly understood. Here, we demonstrate that colonization of the lungs by metastatic breast cancer cells induces an inflammatory phenotype in lung fibroblasts. CXCL9 and CXCL10 are induced in an NFκB-dependent manner in metastasis-associated fibroblasts in response IL-1α and IL-1β secreted by disseminated breast cancer cells. We find that the chemokine receptor CXCR3, that binds CXCL9/10, is expressed in a small subset of breast cancer cells that exhibits greater tumor-initiating ability when co-transplanted with fibroblasts. CXCR3-expressing cancer cells maintain JNK signaling that drives IL-1A/B expression, and thus rendering this subpopulation efficient in both inducing CXCL9/10 in lung fibroblasts and responding to the chemokines. Importantly, disruption of the CXCL9/10-CXCR3 axis significantly reduces metastatic colonization in xenograft and syngeneic mouse models suggesting an essential role of this paracrine crosstalk in metastatic progression and a potential therapeutic vulnerability for the treatment of metastatic breast cancer.

2020-02-17 | GSE121945 | GEO

Macrophage-specific Act1 Knockdown Promoted Adenoma-Adenocarcinoma Transition in Apcmin+/- Mice via Activation of the CXCL9/10-CXCR3 axis

Project description:macrophages involve in colorectal adenocarcinoma transition. Mouse MC38 colorectal cancer cells were co-cultured with BMDM from both anti-Act1 and Wildtype mice. MC38 cells have higher migration speed and express higher EMT markers including Snail, E-cadherins, and Twist after co-culture with anti-Act1 macrophage. Expression profiling by high throughput sequencing highlighted that by co-culturing with MC38 cells, anti-Act1 macrophage increase proinflammatory cytokines secretion and consequently activates cytokines receptor signaling pathway. Specifically, we identified the mechanism where CXCL9/10 from anti-Act1 macrophage interacted with CXCR3 receptor in MC38 cell to promote MC38 migration as well as EMT. Besides, coculturing with MC38 cells enhanced expressions of PD-L1 and MDSCs markers such as Arg1, iNOS, IDO1 in anti-Act1 macrophages. Among activating pathways, we reveal that anti-Act1 macrophage orchestrates NF-kB and STAT3 signaling pathways to upregulate CXCL9/10 secretion and PD-L1 expression. These findings demonstrate that anti-Act1 in macrophage induced a significant shift in MC38 cells gene expression, and modulating the macrophage-cancer is a viable strategy to assist PD-L1 immunotherapy.

2022-09-01 | GSE183971 | GEO

Transcriptomic profiling of CXCL9/10-overexpressing (OE) MDA-MB-231 breast cancer cells upon treatment with CXCR3i or DMSO vehicle

2020-02-17 | GSE137178 | GEO

Glucocorticoids target the CXCL9/10-CXCR3 axis and confer protection against immune-mediated kidney injury

Project description:Glucocorticoids target the CXCL9/10-CXCR3 axis and confer protection against immune-mediated kidney injury

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RNAseq of CD8 T-cells stimulated with CXCR3 chemokines

Project description:G protein-coupled receptors (GPCRs) interact with many transducers like G proteins and β-arrestins. Some GPCR agonists act as “biased agonists” which preferentially activate specific signaling transducers over others, leading to unique signaling profiles. The chemokine system, a subfamily of GPCRs that plays a critical role in inflammatory diseases, serves as an endogenous example of biased agonism where over 50 different chemokines ligands and 20 receptors interact promiscuously. In this study, we sought to determine the three different chemokines of the chemkoine receptor CXCR3 generate different transcriptional responses in primary CD8+ T cells. Using RNAseq on CD8+ T cells stimulated with either vehicle control, CXCL9, CXCL10, or CXCL11, the endogenous chemokines of CXCR3, we found that the CXCR3 chemokines promoted unique transcriptional responses that are predicted to differentially regulate inflammatory pathways. We observed significant changes in global transcriptional activation, detecting approximately 48000 transcripts, 887 of which varied by chemokine treatment. There was a high degree of replicability between biological replicates. The overwhelming majority of differentially expressed genes (DEGs) increased in transcript level following chemokine treatment. Compared to vehicle control, CXCL11 demonstrated the largest number of DEGs. Importantly, CXCL11 and CXCL10 demonstrate unique transcriptional profiles where the majority of DEGs were only found following treatment with each specific chemokine, rather than being shared across chemokines. These data contrast with that observed at CXCL9 – although it promoted a significant amount of transcriptional regulation, approximately 66% of CXCL9-induced DEGs were shared with CXCL11 and/or CXCL10.

2022-07-23 | GSE192679 | GEO

Bacillus subtilis strain:1A1

Project description:Bacillus subtilis strain:1A1 Genome sequencing and assembly

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PRTN3 suppresses cytotoxic immune-cell activation and antitumoral immunity through proteolytic cleavage of CXCL9 in KRAS mutant lung adenocarcinoma

Project description:The intratumoral activity of chemokine system has important roles in cancer immunotherapy strategies.One of the mechanisms of immune checkpoint blocking (ICB)resistance may be the dysfunction of chemokine signaling. Here, we first report that KRAS mutation in LUAD cells up-regulates the expression of protease 3 (PRTN3), that inhibits cytotoxic immune cell activation in the tumor microenvironment by inhibiting the CXCL9/CXCR3 axis, providing an unconventional mechanism for tumor immune escape. Further mechanism studies demonstrated that PRTN3 was up-regulated by c-Myc transcription and secreted into the tumor microenvironment, where CXCL9 was inactivated by proteolysis, and finally result in inhibiting the activation of natural killer (NK) and CD8+ T cells. Meanwhile, samples from LUAD patients with high PRTN3 expression showed low CXCL9 activity. Furthermore, application of a hydrolysis-resistant CXCL9 protein (H-R CXCL9) effectively improves the immunomodulate effect in LUAD patient organoids. Importantly, PRTN3 knockdown increased the susceptibility of KRAS mutant cells to Anti-pd-1 therapy. Thus, we have identified a previously unknown tumor immune-suppressive mechanism and provided an immunotherapeutic target to improve the effectiveness of ICB therapy in KRAS mutant LUAD.

2024-07-13 | GSE271713 | GEO

Macrophage-specific Act1 Knockdown Promoted Adenoma-Adenocarcinoma Transition in Apcmin+/- Mice via Activation of the CXCL9/10-CXCR3 axis

Project description:Macrophage-specific Act1 Knockdown Promoted Adenoma-Adenocarcinoma Transition in Apcmin+/- Mice via Activation of the CXCL9/10-CXCR3 axis

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Transcriptional analysis of murine CXCR3+ vs. CXCR3- peritoneal cavity B cells 8 days following infection with Ehrlichia muris.

Project description:We performed bulk RNA sequencing on murine CXCR3+ and CXCR3-negative live singlet IgM+ IgD-neg CD19+ CD138-neg (B1 B cell-like) peritoneal cavity B cells to compare the transcriptomes of the two populations following i.p. infection with the intracellular bacterium Ehrlichia muris. Total RNA was extracted and sequenced, followed by pseudoalignment, quality assessment, normalization, and analysis of differential gene expression. The CXCR3+ B1 B cell-like population was highly enriched for genes involved in proliferation, metabolism, and cell division, whereas the CXCR3- B1 B cell-like population transcriptionally resembled canonical B1 B cells and did not appear to be proliferative. These results suggest local proliferation of CXCR3+ B cells occurs in the peritoneal cavity during acute infection with an intracellular bacterium.

2022-04-18 | GSE190651 | GEO

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