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CXCR3-expressing macrophages regulate angiogenesis, tumor cell proliferation and immune evasion in hepatocellular carcinoma

ABSTRACT: CXCR3-expressing macrophages regulate angiogenesis, tumor cell proliferation and immune evasion in hepatocellular carcinoma

PROVIDER: PRJNA789900 | ENA |

REPOSITORIES: ENA

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CXCR3-expressing macrophages regulate angiogenesis, tumor cell proliferation and immune evasion in hepatocellular carcinoma

Project description:Chemokine receptor CXCR3 shapes the intrahepatic tumor microenvironment in a highly dynamic manner. Genetic deletion of Cxcr3 has an impact on the development and differentiation of myeloid cells and improves potentially oncogenic properties of tumor-associated macrophages in hepatocellular carcinoma (HCC) bearing mice. This ultimately leads to an increased carcinogenesis.

2024-12-01 | GSE191156 | GEO

Cxcr3 expressing leukocytes are necessary for neurofibroma formation in mice

Project description:Plexiform neurofibroma is a major contributor to morbidity in Neurofibromatosis type I (NF1) patients. Macrophages and mast cells infiltrate neurofibroma, and data from mouse models implicate these leukocytes in neurofibroma development. Anti-inflammatory therapy targeting these cell populations has been suggested as a means to prevent neurofibroma development. Here, we compare gene expression in inflamed nerves from NF1 models which invariably form neurofibroma to those with inflammation driven by EGFR overexpression which rarely progresses to neurofibroma. We find that the chemokine Cxcl10 is uniquely up-regulated in NF1 mice that invariably develop neurofibroma. Global deletion of the Cxcl10 receptor Cxcr3 prevented neurofibroma development in these neurofibroma-prone mice. Cxcr3 expression localized to T cells and dendritic cells (DCs) in both inflamed nerves and neurofibromas. These data support a heretofore unappreciated role for T cells/DCs in neurofibroma initiation.

2018-11-28 | GSE122999 | GEO

Cxcr3 expressing leukocytes are necessary for neurofibroma formation in mice

Project description:Plexiform neurofibroma is a major contributor to morbidity in Neurofibromatosis type I (NF1) patients. Macrophages and mast cells infiltrate neurofibroma, and data from mouse models implicate these leukocytes in neurofibroma development. Anti-inflammatory therapy targeting these cell populations has been suggested as a means to prevent neurofibroma development. Here, we compare gene expression in inflamed nerves from NF1 models which invariably form neurofibroma to those with inflammation driven by EGFR overexpression which rarely progresses to neurofibroma. We find that the chemokine Cxcl10 is uniquely up-regulated in NF1 mice that invariably develop neurofibroma. Global deletion of the CXCL10 receptor, Cxcr3, prevented neurofibroma development in these neurofibroma-prone mice. Cxcr3 expression localized to T cells and dendritic cells (DCs) in both inflamed nerves and neurofibromas. These data support a heretofore unappreciated role for T cells/DCs in neurofibroma initiation.

2019-02-24 | GSE122730 | GEO

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

NOTCH1 orchestrates a multifaceted malignant and immune evasion program in hepatocellular carcinoma

Project description:NOTCH1 orchestrates a multifaceted malignant and immune evasion program in hepatocellular carcinoma

| PRJNA903395 | ENA

Pro-inflammatory Beta Cell Small Extracellular Vesicles Induce Beta Cell Failure Through Activation of the CXCL10/CXCR3 Axis in Diabetes

Project description:Coordinated communication among pancreatic islet cells is necessary for the maintenance of glucose homeostasis. In diabetes, chronic exposure to pro-inflammatory cytokines has been shown to perturb β-cell communication and function. Compelling evidence has implicated extracellular vesicles (EVs) in modulating physiological and pathological responses to β-cell stress. We report that pro-inflammatory β-cell small EVs (cytoEV) induce β-cell dysfunction, promote a pro-inflammatory islet transcriptome, and enhance recruitment of CD8+ T-cells and macrophages. Proteomic analysis of cytoEV revealed an enrichment of the chemokine, CXCL10, with surface topological analysis depicting CXCL10 as membrane-bound on cytoEV to facilitate direct binding to CXCR3 receptors on the surface of β-cells. CXCR3 receptor inhibition reduced CXCL10-cytoEV binding and attenuated β-cell dysfunction, inflammatory gene expression, and leukocyte recruitment to islets. Collectively, this work implicates the significant role of pro-inflammatory β-cell derived small EVs in modulating β-cell function, global gene expression, and antigen presentation through activation of the CXCL10/CXCR3 axis.

2021-08-25 | PXD026998 | Pride

Cxcr3 expressing leukocytes are necessary for neurofibroma formation in mice

Project description:Cxcr3 expressing leukocytes are necessary for neurofibroma formation in mice

| PRJNA507362 | ENA

Cxcr3 expressing leukocytes are necessary for neurofibroma formation in mice

Project description:Cxcr3 expressing leukocytes are necessary for neurofibroma formation in mice

| PRJNA507180 | ENA

T cell receptors repertoire sequencing of the human CD8+ naive subsets (CXCR3-,CXCR3+)

Project description:T cell receptors repertoire sequencing of the human CD8+ naive subsets (CXCR3-,CXCR3+)

| PRJEB31057 | ENA

Cxcl10 and Cxcr3 regulate self-renewal and differentiation of hematopoietic stem cells

Project description:Background: The function of hematopoietic stem cells (HSC) is regulated by HSC internal signaling pathways and their microenvironment. Chemokines and chemokine ligands play important roles in the regulation of HSC function. Yet, their functions in HSC are not fully understood. Methods: We established Cxcr3 and Cxcl10 knockout mouse models (Cxcr3-/- and Cxcl10-/-) to analyze the roles of Cxcr3 or Cxcl10 in regulating HSC function. The cell cycle distribution of LT-HSC was assessed via flow cytometry. Cxcr3-/-and Cxcl10-/-stem/progenitor cells showed reduced self-renewal capacity as measured in serial transplantation assays. To study the effects of Cxcr3 or Cxcl10 deficient bone marrow microenvironment, we transplanted CD45.1 donor cells into Cxcr3-/-or Cxcl10-/- recipient mice (CD45.2) and examined donor-contributed hematopoiesis. Results: Deficiency of Cxcl10 and its receptor Cxcr3 led to decreased BM cellularity in mice, with a significantly increased proportion of LT-HSC. Cxcl10-/- stem/progenitor cells showed reduced self-renewal capacity in the secondary transplantation assay. Notably, Cxcl10-/- donor-derived cells preferentially differentiated into B lymphocytes, with skewed myeloid differentiation ability. Meanwhile, Cxcr3-deficient HSCs demonstrated a reconstitution disadvantage in secondary transplantation, but the lineage bias was not significant. Interestingly, the absence of Cxcl10 or Cxcr3 in bone marrow microenvironment did not affect HSC function. Conclusions: The Cxcl10 and Cxcr3 regulate the function of HSC, including self-renewal and differentiation, adding to the understanding of the roles of chemokines in the regulation of HSC function.

2024-07-25 | GSE272747 | GEO

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