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Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [Nanostring]

ABSTRACT: Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [Nanostring]

PROVIDER: PRJNA1010749 | ENA |

REPOSITORIES: ENA

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Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression

Project description:Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression

| PRJNA1010745 | ENA

Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [PyMT_RNA-Seq]

Project description:Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [PyMT_RNA-Seq]

| PRJNA1010748 | ENA

Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [BMDM_RNA-Seq]

Project description:Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [BMDM_RNA-Seq]

| PRJNA1010750 | ENA

Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [Nanostring]

Project description:Due to the limited efficacy of Immune checkpoint blockade (ICB) in mammary solid tumors alternative strategies are required. We demonstrated that cholesterol homeostasis plays a significant role in myeloid immune function and breast cancer progression. In this study, we focus on NR0B2. We conducted both in vitro and in vivo studies along with developing a small molecule agonist. NR0B2 functions within myeloid immune cells as a regulator of the NLRP3 inflammasome, which further facilitates T cell differentiation away from immune-suppressive regulatory T cells (Treg). Furthermore, this signaling pathway was demonstrated to attenuate breast tumor growth and metastasis in mouse models.

2023-09-04 | GSE241917 | GEO

Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-04 | GSE241918 | GEO

Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [BMDM_RNA-Seq]

2023-09-04 | GSE241916 | GEO

Re-education of myeloid immune cells to reduce regulatory T cell expansion and impede breast cancer progression [PyMT_RNA-Seq]

2023-09-04 | GSE241915 | GEO

Re-education of tumor-associated macrophages by CXCR2 blockade drives senescence and tumor inhibition in advanced prostate cancer

2019-06-03 | GSE125273 | GEO

Re-education of tumor-associated macrophages by CXCR2 blockade drives senescence and tumor inhibition in advanced prostate cancer

Project description:Tumor-associated macrophages (TAMs) represent a major component of the tumor microenvironment that supports tumorigenesis. Here we found that prostate tumors are strongly infiltrated by TAMs expressing the C-X-C chemokine receptor type 2 (CXCR2). Pharmacological blockade of the CXCR2 receptor by a selective antagonist promoted the re-education of TAMs towards a pro-inflammatory phenotype. Strikingly, CXCR2 knockout monocytes infused in Ptenpc-/-; Trp53pc-/- mice preferentially differentiatied in TNFα-releasing pro-inflammatory macrophages leading to senescence induction and tumor inhibition. Moreover, tumor cells harboring PTEN deletion were more sensitive to TNFα-induced senescence, when compared to PTEN WT tumors, due to increased levels of TNFR1. Our results identify TAMs as a target in prostate cancer therapy and describe a novel therapeutic strategy based on CXCR2 blockade to harness the anti-tumorigenic potential of macrophages against this disease.

2019-12-10 | GSE124058 | GEO

Endothelial Rbpj is essential for the education of tumor-associated macrophages

Project description:Epithelial ovarian cancer (EOC) is one of the most lethal gynecological cancers worldwide. EOC cells educate tumor-associated macrophages (TAMs) through CD44-mediated cholesterol depletion to generate an immunosuppressive tumor microenvironment (TME). In addition, tumor cells frequently activate Notch1 receptors on endothelial cells (ECs) to facilitate metastasis. However, little is known whether the endothelium would also influence the education of recruited monocytes. Here, we report that canonical Notch signaling through RBPJ in ECs is an important player in the education of TAMs and EOC progression. Deletion of Rbpj in the endothelium of adult mice reduced infiltration of monocyte-derived macrophages into the TME of EOC and prevented the acquisition of a typical TAM gene signature. This was associated with stronger cytotoxic activity of T cells and decreased tumor burden. Mechanistically, we identified CXCL2 as a novel Notch/RBPJ target gene. This angiocrine factor regulates the expression of CD44 on monocytes and subsequent cholesterol depletion of TAMs. Bioinformatic analysis of ovarian cancer patient data showed that increased CXCL2 expression is accompanied by higher expression of CD44 and TAM education. As such, EOC cells employ the tumor endothelium to secrete CXCL2 in order to facilitate an immunosuppressive microenvironment.

2022-09-15 | GSE213371 | GEO

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