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The CX3CL1-CX3CR1 chemokine axis can contribute to tumor immune evasion and blockade with a novel CX3CR1 monoclonal antibody enhances responses to anti-PD-1 immunotherapy [CT26]

ABSTRACT: To investigate the imunoresistance programs regulated by the CX3CL1-CX3CR1 axis, we treated CT26 mouse tumor cell line with CX3CL1, CX3CL1 + IFN-γ, IFN-γ, and no treatment

ORGANISM(S): Mus musculus

PROVIDER: GSE215269 | GEO | 2023/09/01

REPOSITORIES: GEO

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The CX3CL1-CX3CR1 chemokine axis can contribute to tumor immune evasion and blockade with a novel CX3CR1 monoclonal antibody enhances responses to anti-PD-1 immunotherapy [CT26]

Project description:The CX3CL1-CX3CR1 chemokine axis can contribute to tumor immune evasion and blockade with a novel CX3CR1 monoclonal antibody enhances responses to anti-PD-1 immunotherapy [CT26]

| PRJNA889457 | ENA

Differential regulation by CX3CR1 ligands CX3CL1 and CCL26 on mouse bone marrow-derived macrophages

Project description:We studied the effect of ligation on chemokine receptor CX3CR1 in the mouse bone marrow-derived macrophages (BMDM). We compared transcriptional profiles of BMDM treated with CX3CL1 and those of CCL26 to test if these two CX3CR1 ligands regulate differently.

2023-01-29 | GSE166291 | GEO

Back-signaling from CX3CL1 regulates neurogenesis during development and in the adult mouse

Project description:CX3CL1 was discovered as a chemokine, and is best known to function via interaction with its receptor CX3CR1. However, in this study, we report a unique role of CX3CL1 that is independent from this pathway. We show that CX3CL1 is naturally shedded by both α- and β-secretase. The membrane-anchored C-terminal fragment is further cleaved by γ-secretase to release the CX3CL1 intracellular domain (CX3CL1-ICD), which is translocated into the cell nucleus to control gene expression. Among the regulated genes, we noted prominent induction of TGFβ2/TGFβ3 signaling in cultured cells by CX3CL1-ICD. Mice overexpressing only the C-terminal fragment (Tg-CX3CL1-ct) strongly induced TGFβ3 expression, as evidenced by Western and RNAseq analyses. Phenotypically, Tg-CX3CL1-ct mice exhibited enhanced neurogenesis both during development and in adulthood. Enhanced adult neurogenesis was seen in both the subgranular zone and the subventricular zone. Together, we demonstrate that CX3CL1-ct has a back-signaling function by enhancing neurogenesis through TGFβ3 and other genes important for neurogenesis. Induction CX3CL1 back signaling may be a promising novel mechanism to replenish neuronal loss.

2019-06-08 | GSE129722 | GEO

CX3CL1 and IL-15 Promote CD8 T Cell Chemoattraction in HIV and in Atherosclerosis

Project description:Atherosclerotic cardiovascular disease (ASCVD) remains an important cause of morbidity in the general population and risk for ASCVD is increased approximately 2-fold in persons living with HIV infection (PLWH). This risk is linked to elevated CD8 T cell counts that are abundant in atherosclerotic plaques and have been implicated in disease pathogenesis yet the mechanisms driving T cell recruitment to and activation within plaques are poorly defined. Here we investigated the role of CD8 T cells in atherosclerosis in a non-human primate model of HIV infection and in the HIV-uninfected elderly; we sought to identify factors that promote the activation, function, and recruitment to endothelium of CX3CR1+ CD8 T cells. We measured elevated expression of CX3CL1 and IL-15, and increased CD8 T cell numbers in the aortas of rhesus macaques infected with SIV or SHIV, and demonstrated similar findings in atherosclerotic vessels of HIV-uninfected humans. We found that recombinant TNF enhanced the production and release of CX3CL1 and bioactive IL-15 from aortic endothelial cells, but not from aortic smooth muscle cells. IL-15 in turn promoted CX3CR1 surface expression on and TNF synthesis by CD8 T cells, and IL-15-treated 60 CD8 T cells exhibited enhanced CX3CL1-dependent chemoattraction toward endothelial cells in vitro. Finally, we show that CD8 T cells in human atherosclerotic plaques have an activated, resident phenotype consistent with in vivo IL-15 and CX3CL1 exposure. In this report, we define a novel model of CD8 T cell involvement in atherosclerosis whereby CX3CL1 and IL-15 operate in tandem within the vascular endothelium to promote infiltration by activated CX3CR1+ memory CD8 T cells that drive further endothelial activation via TNF. We propose that these interactions are prevalent in aging and in PLWH, populations where circulating activated CX3CR1+ CD8 T cell numbers are often expanded.

2020-10-12 | GSE154644 | GEO

Differential regulation by CX3CR1 ligands CX3CL1 and CCL26 on mouse bone marrow-derived macrophages

Project description:Differential regulation by CX3CR1 ligands CX3CL1 and CCL26 on mouse bone marrow-derived macrophages

| PRJNA700068 | ENA

Cx3cl1 expression in the adipose tissue is downregulated during development of obesity

Project description:To assess changes in expression level of various chemokines and their receptors on diet-induced obesity, we analysed gene expression in adipose tissue of C56BL/6J mice fed a high-fat (HF) diet or normal chow diet for 8 weeks. HF diet-induced obese (DIO) mice showed adipose tissue inflammation and insulin resistance. Comprehensive gene expression analysis showed that MCP-1–CCR2 and CCL5–CCR5 signalling in epididymal white adipose tissue (eWAT) were enhanced during the development of obesity. Surprisingly, the gene expression of Cx3cl1 was decreased in the eWAT of DIO mice compared with lean mice. While Cx3cr1 expression showed no significant difference between DIO and lean mice. Decreased CX3CL1-CX3CR1 signalling in adipose tissue may also be involved in the development of obesity-induced adipose tissue inflammation and insulin resistance.

2021-04-01 | GSE167311 | GEO

Mononuclear phagocytes in muscle after notexin injury in C57Bl/6, Cx3cr1-/-, Ccl2-/-,Cx3cr1-/-Ccl2-/- mice

Project description:Muscle injury triggers inflammation in which infiltrating mononuclear phagocytes are crucial for tissue regeneration. The interaction of the CCL2/CCR2 and CX3CL1/CX3CR1 chemokine axis that guides phagocyte infiltration is incompletely understood. Here, we show that CX3CR1 deficiency promotes muscle repair and rescues Ccl2-/- mice from impaired muscle regeneration as a result of altered macrophage function, not infiltration. Transcriptomic analysis of muscle mononuclear phagocytes reveals that Apolipoprotein E (ApoE) is up-regulated in mice with efficient regeneration. ApoE treatment enhances phagocytosis by mononuclear phagocytes in vitro, and restores phagocytic activity and muscle regeneration in Ccl2-/- mice. Because CX3CR1 deficiency may compensate for defective CCL2-dependant monocyte recruitment by modulating ApoE-dependent macrophage phagocytic activity, targeting CX3CR1 expressed by macrophages might be a powerful therapeutic approach to improve muscle regeneration.

2015-09-29 | GSE73473 | GEO

RNA sequencing comparison of CXCR3+ and CX3CR1+ CD4+ epitope specific T cells from Se-infected mice.

Project description:Interferon-γ (IFN-γ)-producing CD4+ T helper-1 (Th1) cells are critical for protection from microbes that infect the phagosomes of myeloid cells. We assessed Th1 cell generation in vivo by studying antigen-specific CD4+ T cells during infection with the phagosomal pathogen Salmonella enterica. We found that this infection induced two varieties of Th1 cells, one expressing CXCR3 and one expressing CX3CR1. We performed RNA sequencing on these two types of Th1 cells that were specific for the LpdAp:I-Ab epitope from B6 x 129 F1 mice 30 days after Salmonella enterica infection to gain information about the differences between these types of Th1 cells and how those differences might relate to protective immunity. We report results for CXCR3+ CX3CR1- and CXCR3- CX3CR1+ LpdAp:I-Ab-tetramer binding cells.

2021-03-18 | GSE168300 | GEO

TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

Project description:TCR variable regions transcripts of three CT26-shppp2r1a samples and three CT26-scr samples

2021-11-20 | GSE189092 | GEO

Anti-CX3CL1 (fractalkine) monoclonal antibody attenuates lung and skin fibrosis in sclerodermatous graft-versus-host disease mouse model

Project description:To assess the preclinical utility and functional mechanism of intraperitoneal anti-CX3CL1 mAb therapy in the skin and lung fibrosis, sclerodermatous chronic graft-versus-host disease (Scl-cGVHD) model mice were analyzed by RNA-sequencing assays.

2024-05-03 | GSE227285 | GEO

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