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Spatial crosstalk modeling of the tumor microenvironment uncovers CCR5-mediated glia-to-glia signaling as a key regulator of brain metastases

ABSTRACT: Spatial crosstalk modeling of the tumor microenvironment uncovers CCR5-mediated glia-to-glia signaling as a key regulator of brain metastases

PROVIDER: PRJNA1235279 | ENA |

REPOSITORIES: ENA

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Spatial crosstalk modeling of the tumor microenvironment uncovers CCR5-mediated glia-to-glia signaling as a key regulator of brain metastases

Project description:Glial cells play a critical role in shaping the tumor microenvironment in brain metastases, facilitating disease progression through complex tumor-glial and distinct glia-to-glia signaling pathways. To investigate these interactions, we conducted RNA sequencing of astrocytes, microglia, and oligodendrocytes at various stages of brain metastasis progression, combined with spatial transcriptomics and crosstalk analysis using the CCCExplorer tool. Our analysis uncovered that while glial cells converge on tumor-promoting pathways such as Ras and Gap junction signaling in tumor cells, they also engage in distinct autocrine and paracrine signaling critical for their own communication. Unique ligand-receptor pairs including OSM-OSMR, CCL4-CCR5, CXCL16-CXCR6, IL1A/B-IL1R, and TNF-TNFR were identified as drivers of glial crosstalk, which sustains the tumor-supportive niche. Targeting CCL4-CCR5-mediated glial signaling with maraviroc, an FDA-approved antiviral drug, reduced brain metastasis progression by 62% (p=0.004) without direct cytotoxicity to tumor cells. These findings highlight the novelty of targeting distinct glial autocrine and paracrine signaling as a therapeutic approach, shifting the focus from tumor cells to disrupting the glial niche that supports brain metastasis growth.

2025-08-20 | GSE291813 | GEO

Spatial crosstalk modeling of the tumor microenvironment uncovers CCR5-mediated glia-to-glia signaling as a key regulator of brain metastases

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Project description:OT-I T cells were exposed to CpG ODN-activated CCR5ko Lymph nodes for 6 h, stained for surface CCR5 and FACS-sorted into CCR5+ and CCR5- fractions In the study presented here freshly isolated OT1 T cells were exposed for 6h at 37oC to teased-out CpG ODN-activated CCR5ko LNs in 96-well plates and stained for surface CCR5 before sorting into CCR5+ (Hua2) and CCR5- (Hua1) fractions. High quality total RNA isolated from each cell fraction using TRIZOL and Qiagen RNEasy kit per manufacture's recommendation was subjected to microarray analysis using the Affymetrix Mouse Gene ST 1.0 array chip to discover differentially expressed genes.

2016-01-14 | E-GEOD-76820 | biostudies-arrayexpress

People with HIV have higher percentages of circulating CCR5+ CD8+ T cells and lower percentages of CCR5+ regulatory T cells

Project description:CCR5 is the main HIV co-receptor. We aimed to (1) compare CCR5 expression on immune cells between people living with HIV (PLHIV) using combination antiretroviral therapy (cART) and HIV-uninfected controls, (2) relate CCR5 expression to viral reservoir size and (3) assess detereminants of CCR5 expression. Percentages of CCR5 positive cells (%) and CCR5 mean fluorescence intensity (MFI) assessed by flow cytometry in monocytes and lymphocyte subsets were correlated to host factors, HIV-1 cell-associated (CA)-RNA and CA-DNA, plasma inflammation markers and metabolites.

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Differential Gene expression in CCR5+ versus CCR5- OT-I T cells

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CCR5-blockade in Metastatic Colorectal Cancer

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Project description:Sequencing of 9kb of the CCR5 genomic locus in 15 patients who naturally control HIV infection

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CCR5 promotes the migration of CD8+ T cells to the leishmanial lesions

Project description:Cytolytic CD8+ T cells mediate immunopathology in cutaneous leishmaniasis without controlling parasites. Here, we identify factors involved in CD8+ T cell migration to the lesion that could be targeted to ameliorate disease severity. CCR5 was the most highly expressed chemokine receptor in patient lesions, and the high expression of CCL3 and CCL4, CCR5 ligands, was associated with delayed healing of lesions. To test the requirement for CCR5, Leishmania-infected Rag1-/- mice were reconstituted with CCR5-/- CD8+ T cells. We found that these mice developed smaller lesions accompanied by a reduction in CD8+ T cell numbers compared to controls. We confirmed these findings by showing that the inhibition of CCR5 with maraviroc, a selective inhibitor of CCR5, reduced lesion development without affecting the parasite burden. Together, these results reveal that CD8+ T cells migrate to leishmanial lesions in a CCR5-dependent manner and that blocking CCR5 prevents CD8+ T cell-mediated pathology.

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