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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity

ABSTRACT: Single cell sequence (SC-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. MTC-Q1 oral cancer cells were orthotopic injection in C57BL/6 mice. CD45+ immune cells has been isolated, analyzed and sequenced by dropped based scRNA-seq, cDNA were sequenced by Illumina Novaseq 6000.

ORGANISM(S): Mus musculus

PROVIDER: GSE190111 | GEO | 2023/07/09

REPOSITORIES: GEO

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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity V

Project description:Bulk RNA sequence (RNA-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. MTC-Q1 oral cancer cells were orthotopic injection into C57BL/6J mice. tumor tissue has been isolated (~ 100 mm3) and total RNA were extracted by Trizol, followed by cDNA were sequenced by Illumina NextSeq 550.

2023-07-09 | GSE193054 | GEO

Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity IV

2023-07-09 | GSE193051 | GEO

Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity III

Project description:Bulk RNA sequence (RNA-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. MTC-Q1 oral cancer cells were orthotopic injection in C57BL/6 mice. CD45-negatve cells has been isolated and RNA were extracted by Trizol, followed by cDNA were sequenced by Illumina NextSeq 550.

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Interleukin-10/CSF1R fusion protein rejuvenates the exhausted T cells for executing antitumor activity II

Project description:Bulk RNA sequence (RNA-seq) has been used to explore the effect of IL10/CSF1R fusion protein modulation in tumor microenvironment. Four groups were analyzed which contain Ctrl, CSF1R, IL10 and BF10. 4T1 breast cancer cells were orthotopic injection into Balb/c mice. tumor tissue has been isolated (~ 100 mm3) and total RNA were extracted by Trizol, followed by cDNA were sequenced by Illumina NextSeq 550.

2023-07-09 | GSE193045 | GEO

Single cell sequence of tumor infiltrated immune cells after cisplatin treatment in control or miR-21 KO in mouse oral cancer model

Project description:Single cell sequence (SC-seq) has been used to explore the effect of miR-21-modulated chemotherapy-induced tumor microenvironment change. MTC-Q1 WT or MTC-Q1 miR-21 KO cells were subcutaneously injected into C57BL/6 mice. CD45+ immune cells has been isolated after cisplatin injection. The isolated immune cell were sequenced by dropped based scRNA-seq, cDNA were sequenced by Illumina Novaseq 6000.

2022-08-29 | GSE172326 | GEO

Gene expression data of CSF1R antibody-treated myeloma-associated macrophages

Project description:Colony-stimulating factor 1 receptor (CSF1R) signaling controls MФ differentiation and function, and blocking CSF1R exerts antitumor effects in solid tumors. We examined the effects of CSF1R blockade on multiple therapy. Our results showed that CSF1R blockade inhibited the differentiation, proliferation and survival of M2 and myeloma-associated MФs (MAMs). Microarray was used for determining CS7 effect on polarization of MAMs. We used microarrays to detail the global programme of gene expression underlying polarizaiton of myeloma-associated macrophages by CSF1R antibody treatment and identified distinct classes of polarization-related genes during this process.

2017-06-30 | GSE99393 | GEO

Effect of CSF1R targeting on human macrophages in normoxia and hypoxia

Project description:CSF1R is a receptor involved in differentiation and survival of macrophages. We designed this study to explore the consequences of CSF1R targeting on human macrophage transcriptome. We also seek to explore the influence of oxygen environnment on the consequences of CSF1R blocakde . Our data provide an extensive characterization of the various pathways connected to CSF1/CSF1R pathway in human macrophages.

2024-04-18 | GSE263919 | GEO

Effect of CSF1R inhibition in tumor macrophages on gene expression in metastatic epithelial cells

Project description:Metastasis is the primary cause of mortality in breast cancer patients. Tumor associated macrophages (TAMs) are active collaborators in mediating several steps of the tumor metastatic cascade, but the molecular details governing this collaboration remain ill-defined. Colony Stimulating Factor 1 (CSF1), a factor critical for macrophage differentiation and survival, functions to recruit TAMs to the primary tumor site, and anti-CSF1 therapies are in clinical trials.In this study, we tested the effect of inhibiting CSF1 signaling in macrophages on gene expression in metastatic tumor cells in mouse models of breast cancer metastasis. Tumor cells were sorted from lung metastases from control and CSF1R inhibitor treated mice. Several pro-tumor processes were significantly affected by CSF1R inhibitor treatment, including angiogenesis and tumor cell proliferation. In addition, a 29 gene signature derived from this data could retrospectively predict survival in a cohort of luminal B breast cancer patients. Collectievly, our results highlight the utility of employing CSF1R inhibitors for the treatment of metastatic breast cancer. GFP tagged MVT1 metastatic mammary tumor cells were injected intravenously into FVB/N mice. Mice were gavaged with the CSF1R inhibitor GW2580 or vehicle starting one week post injection. GFP tagged tumor cells were sorted from metastatic tumor bearing lungs 1 and 2 weeks post injection from 2 vehicle treated mice for each. These are denoted 1_week_WT and 2_week_WT respectively. GFP tagged tumor cells were simultaneously sorted from mice gavaged with GW2580. These samples are denoted 2_week_GW. RNA was extracted and gene expression profiling was performed using the Affymetrix Mouse Genome 430 2.0 Array platform.

2014-03-13 | E-GEOD-55855 | biostudies-arrayexpress

Gene expression in murine pancreatic tumor tissues in response to the blockade of macrophage colony-stimulating factor receptor (CSF1R) signal

Project description:Analysis of responses induced upon the blockade of CSF1R signaling at the gene expression level. Hypothesis of this study was that CSF1R signal blockade alters the local immune responses in a murine pancreatic tumor model. Results provide important information on changes in the immune responses in the tumor microenvironment. Total RNA obtained from whole mouse pancreatic tumor tissues after vehicle or CSF1Ri treatment for 8 days

2014-05-15 | E-GEOD-57686 | biostudies-arrayexpress

CSF1R inhibition promotes neuroinflammation and behavioural deficits during graft-versus-host disease in mice.

Project description:Chronic graft-versus-host disease (cGVHD) remains a significant complication of allogeneic hematopoietic stem cell transplantation. Central nervous system (CNS) involvement is becoming increasingly recognised, where brain-infiltrating donor MHC class II+ bone marrow-derived macrophages (BMDM) drive pathology. BMDM are also mediators of cutaneous and pulmonary cGVHD, and clinical trials assessing the efficacy of antibody blockade of colony-stimulating factor 1 receptor (CSF1R) to deplete macrophages are promising. We hypothesised that CSF1R antibody blockade may also be a useful strategy to prevent/treat CNS cGVHD. Increased blood-brain barrier permeability during acute GVHD (aGVHD) facilitated CNS antibody access and microglia depletion by anti-CSF1R treatment. However, CSF1R blockade early post-transplant unexpectedly exacerbated aGVHD neuroinflammation. In established cGVHD, vascular changes and anti-CSF1R efficacy were more limited. Anti-CSF1R-treated mice retained donor BMDM, activated microglia, CD8+ and CD4+ T cells, and local cytokine expression in the brain. These findings were recapitulated in GVHD recipients where CSF1R was conditionally depleted in donor CX3CR1+ BMDM. Notably, inhibition of CSF1R signalling post-transplant failed to reverse GVHD-induced behavioural changes. Moreover, we observed aberrant behaviour in non-GVHD control recipients administered anti-CSF1R blocking antibody and naïve mice lacking CSF1R in CX3CR1+ cells, revealing a novel role for homeostatic microglia and indicating that ongoing clinical trials of CSF1R inhibition should assess neurological adverse events in patients. In contrast, transfer of Ifngr-/- grafts could reduce MHC class II+ BMDM infiltration, resulting in improved neurocognitive function. Our findings highlight unexpected neurological immune toxicity during CSF1R blockade and provide alternative targets for the treatment of cGVHD within the CNS.

2023-10-18 | GSE245360 | GEO

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