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Gene expression profiling of CD45+CD11b+F4/80high macrophages and CD45+TCRbeta+CD8+ T cells in MC38 tumor of WT, muMt-/- or muMt-/- mice implanted with GABA pellet

ABSTRACT: We characterized the tumor-infiltrating macrophages and CD8 T cells, and we found a pro-inflammatory signature of those cells in muMt-/- mice compared to those in WT mice. Furthermore, many target genes of inflammatory cytokines, such as the TNF target genes, highly expressed in muMt-/- mice, were downregulated by exogenous of GABA.

ORGANISM(S): Mus musculus

PROVIDER: GSE169543 | GEO | 2021/09/02

REPOSITORIES: GEO

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Gene expression profiling of CD45+CD11b+F4/80high macrophages and CD45+TCRbeta+CD8+ T cells in MC38 tumor of WT, muMt-/- or muMt-/- mice implanted with GABA pellet

Project description:Gene expression profiling of CD45+CD11b+F4/80high macrophages and CD45+TCRbeta+CD8+ T cells in MC38 tumor of WT, muMt-/- or muMt-/- mice implanted with GABA pellet

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Gene expression profiling of CD45+CD11b+F4/80high macrophages in MC38 tumor of WT mice injected with DMSO or picrotoxin

Project description:We characterized tumor-associated macrophages and found a pro-inflammatory signature of those cells in picrotoxin-treated mice compared to those in control mice (DMSO).

2021-09-02 | GSE183246 | GEO

ILC2s expanded by exogenous IL-33 regulate CD45+CD11b+F4/80high macrophage polarization to alleviate hepatic ischemia-reperfusion injury.

Project description:Hepatic ischemia-reperfusion injury (IRI) is an adverse consequence of hepatectomy or liver transplantation. Recently, immune mechanisms involved in hepatic IRI have attracted increased attention of investigators working in this area. In specific, group 2 innate lymphoid cells (ILC2s), have been strongly implicated in mediating type 2 inflammation. However, their immune mechanisms as involved with hepatic IRI remain unclear. Here, we reported that the population of ILC2s is increased with the development of hepatic IRI as shown in a mouse model in initial stage. Moreover, M2 type CD45+CD11b+F4/80high macrophages increased and reached maximal levels at 24 h followed by a significant elevation in IL-4 levels. We injected exogenous IL-33 into the tail vein of mice as a mean to stimulate ILC2s production. This stimulation of ILC2s resulted in a protective effect upon hepatic IRI along with an increase in M2 type CD45+CD11b+F4/80high macrophages. In contrast, depletion of ILC2s as achieved with use of an anti-CD90.2 antibody substantially abolished this protective effect of exogenous IL-33 and M2 type CD45+CD11b+F4/80high macrophage polarization in hepatic IRI. Therefore, this exogenous IL-33 induced potentiation of ILC2s appears to regulate the polarization of CD45+CD11b+F4/80high macrophages to alleviate IRI. Such findings provide the foundation for the development of new targets and strategies in the treatment of hepatic IRI.

| S-EPMC9372719 | biostudies-literature

Analysis of LPS stimulation on F480low CD11b High Macrophages from WT and muMT KO mice

Project description:Single cell suspensions from WT or muMT KO mice were stimulated with LPS for 2 hours after which macrophages were sorted

2022-11-01 | GSE139854 | GEO

Gene expression profile of mouse CD206+F4/80+CD11b+ M2-like macrophages

Project description:Characterisation of M2-like macrophage in terms of gene expression level. The hypothesis tested in the present study was that M2-like macrophages in myocardial infarction (MI) heart have upregulation of genes relevant to cardiac repair. The results obtained showed tha various tanti-inflammatory and reparative genes were upregulated in M2-like macrophage from MI heart compared to those from intact hearts. M2-like macrophages from the heart (either MI or intact) were distinct from those in the peritoneal cavity.

2017-06-14 | GSE69879 | GEO

Gene expression profiling of CD45+CD11b+F4/80high macrophages in MC38 tumor of WT mice injected with DMSO or picrotoxin

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CD45+ single cell transcriptomes in the MC38 tumor microenvironment

Project description:Colorectal cancer (CRC) continues to increase globally, thus identification of mechanisms that prevent cancer are sorely needed. The microbiota has emerged as a key driver of CRC pathogenesis; however, little is known regarding how specific microbes might prevent CRC. Using transplantation of the microbiota from individuals with or without CRC into germfree mice, we identified that the microbiota harbored by non-diseased individuals can reduce tumor formation and Bacteroides uniformis was a potentially protective member of the microbiota. Single cell sequencing of CD45+ immune cells within the MC38 tumor shows a change in T and NK cell populations with B. uniformis treatment. T cell deficient mice were still protected from CRC in response to B. uniformis treatment, while NK cell depletion eradicated microbe-mediated protection. B. uniformis is reduced in individuals with CRC and thus our data identify B. uniformis as a microbe enriched in healthy individuals that can reduce tumor formation through enhanced NK cell activity.

2024-01-01 | GSE234875 | GEO

Therapeutic efficacy of plant-produced Nivolumab in transgenic C57BL/6-hPD-1 mouse implanted with MC38 colon cancer.

Project description:The therapeutic blockade of inhibitory PD-1 signaling has emerged as an effective approach for cancer immunotherapy. Nivolumab (Opdivo®), a monoclonal antibody (mAb) targeting the PD-1 immune checkpoint, is approved for treatment of several cancer indications. It functions by blocking the PD-1-mediated T-cell inhibition thus reinstating anticancer immune responses. Tremendous advances in plant biotechnology offer an alternative and economical strategy to produce therapeutic mAbs for immune-based therapies. In this study, recombinant anti-PD-1 Nivolumab was produced in Nicotiana benthamiana and the plant-produced anti-PD-1 mAb was exploited for cancer treatment in syngeneic mice model C57BL/6 mice that were used to test the antitumor efficacy of plant produced Nivolumab, along with commercial Opdivo®. C57BL/6 syngeneic mice treated with plant produced anti-PD-1 mAb exhibited reduction in the growth of established MC38 tumors. The plant produced Nivolumab treatment showed 82.9% antitumor effect in decreasing the tumor volume along with 50% tumor-free mice, whereas Opdivo® showed 90.26% reduction in volume without any tumor-free mice. Finally, plant-derived anti-PD-1 therapy was also well tolerated in tumor-bearing mice that correlated with no significant body weight changes. Overall, our plant-produced Nivolumab elicits significant inhibition of tumor growth in vivo and provides a proof-of-concept for the production of immunotherapy targeting PD-1.

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10x Genomics single cell RNA-sequencing of sorted CD45+ Ly6G- CD11b+ F4/80+ tumour-associated macrophages from murine mammary tumours

Project description:Singe-cell transcriptomic profiling of sorted tumour-associated macrophage cells from mouse mammary adenocarcinomas

2021-11-02 | GSE160641 | GEO

CXCL17 expression by tumor cells recruits CD11b+Gr1 high F4/80- cells and promotes tumor progression.

Project description:BackgroundChemokines are involved in multiple aspects of pathogenesis and cellular trafficking in tumorigenesis. In this study, we report that the latest member of the C-X-C-type chemokines, CXCL17 (DMC/VCC-1), recruits immature myeloid-derived cells and enhances early tumor progression.Methodology/principal findingsCXCL17 was preferentially expressed in some aggressive types of gastrointestinal, breast, and lung cancer cells. CXCL17 expression did not impart NIH3T3 cells with oncogenic potential in vitro, but CXCL17-expressing NIH3T3 cells could form vasculature-rich tumors in immunodeficient mice. Our data showed that CXCL17-expressing tumor cells increased immature CD11b(+)Gr1(+) myeloid-derived cells at tumor sites in mice and promoted CD31(+) tumor angiogenesis. Extensive chemotactic assays proved that CXCL17-responding cells were CD11b(+)Gr1(high)F4/80(-) cells (? 90%) with a neutrophil-like morphology in vitro. Although CXCL17 expression could not increase the number of CD11b(+)Gr1(+) cells in tumor-burdened SCID mice or promote metastases of low metastatic colon cancer cells, the existence of CXCL17-responding myeloid-derived cells caused a striking enhancement of xenograft tumor formation.Conclusions/significanceThese results suggest that aberrant expression of CXCL17 in tumor cells recruits immature myeloid-derived cells and promotes tumor progression through angiogenesis.

| S-EPMC3430639 | biostudies-literature

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