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

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

PROVIDER: PRJNA1010750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25794800.fastq.gz	Fastqsanger.gz
	SRR25794801.fastq.gz	Fastqsanger.gz
	SRR25794802.fastq.gz	Fastqsanger.gz
	SRR25794803.fastq.gz	Fastqsanger.gz
	SRR25794804.fastq.gz	Fastqsanger.gz

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

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

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

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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.

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

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

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

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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.

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Transcriptomic signature associated with education in uterine Natural Killer cells during pregnancy

Project description:Uterine natural killer (uNK) cells regulate vascular changes crucial for placental function and fetal growth. The functional capacity of uNK cells is shaped by their education status. To explore the mechanisms of uNK cell education, we isolated NKG2A+ and Ly49C/I+ educated uNK cells and compared their transcriptomes to uneducated NKG2A-Ly49C/I- uNK cells.

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