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Cxcr3 promotes protection from colorectal cancer liver metastasis by driving NK infiltration and plasticity

ABSTRACT: Cxcr3 promotes protection from colorectal cancer liver metastasis by driving NK infiltration and plasticity

PROVIDER: PRJNA1108698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28927800_1.fastq.gz	Fastqsanger.gz
	SRR28927800_2.fastq.gz	Fastqsanger.gz
	SRR28927801_1.fastq.gz	Fastqsanger.gz
	SRR28927801_2.fastq.gz	Fastqsanger.gz
	SRR28927802_1.fastq.gz	Fastqsanger.gz

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Cxcr3 promotes protection from colorectal cancer liver metastasis by driving NK infiltration and plasticity

Project description:The anti-metastatic activity of NK cells is well established in several cancer types, but the mechanisms underlying NK cell metastasis infiltration and acquisition of anti-tumor characteristics remain unclear. Herein, we investigate the cellular and molecular factors required to facilitate the generation of an ILC1-like CD49a+NK cell population within the liver metastasis environment in orthotopic mouse models of colorectal cancer (CRC). We show that CD49a+NK cells have the highest cytotoxic capacity among metastasis-infiltrating NK cells in the MC38 mouse model. Furthermore, the chemokine receptor CXCR3 promotes CD49a+NK cell accumulation and persistence in metastasis where NK cells co-localize with macrophages in CXCL9 and CXCL10 rich areas. We confirmed the accumulation of CXCR3+ NK cells in metastatic samples mined from a published sc-RNAseq dataset of a cohort of treatment-naïve CRC patients. Conditional deletion of Cxcr3 in NKp46+ cells and antibody-mediated depletion of metastasis-associated macrophages markedly impair CD49a+NK cell development, indicating that CXCR3 and macrophages contribute to efficient NK cell localization and polarization in liver metastasis. Conversely, CXCR3neg NK cells maintain a CD49a- phenotype in metastasis with reduced parenchymal infiltration and tumor killing capacity. Furthermore, CD49a+NK cell accumulation is impaired in an independent SL4-induced CRC metastasis model, which fails to accumulate CXCL9+ macrophages. Together, our results highlight a role for CXCR3/ligand axis in promoting macrophage-dependent NK cell accumulation and functional sustenance in liver metastasis from colorectal cancer.

2025-03-14 | GSE266900 | GEO

Cxcr3 promotes protection from colorectal cancer liver metastasis by driving NK cell infiltration and plasticity.

Project description: Not available

| S-EPMC12126236 | biostudies-literature

Voluntary exercise suppresses tumor growth through exercise-directed recruitment and intratumoral infiltration of NK cells

Project description:Voluntary exercise reduces the risk of cancer and lowers the risk of disease recurrence. Yet the mechanisms for this protection remain to be elucidated. Here we demonstrate that exercise halves tumor growth through an exercise-dependent mobilization and intratumoral infiltration of NK cells in malignant melanoma. Using voluntary wheel running, we show that exercise prior to and during B16 tumor challenge reduced tumor growth by 67%, and this reduction was associated with increased inflammation and immune cell infiltrates, especially NK cells, in the tumors from exercising mice. Depletion of NK cells blunted the exercise-dependent reduction in tumor growth. Moreover, during exercise, NK cells were engaged through an epinephrine-dependent mobilization to the circulation and redistributed to peripheral tissues through an IL-6 dependent mechanism. This study highlights the importance of exercise-dependent immune regulation in the control of malignant melanoma Gene expression profile of melanoma tumor tissue from two groups of exercise and non-exercise mice

2016-07-21 | E-GEOD-62628 | biostudies-arrayexpress

CXCR3 ameliorates neutrophils-dependent disease severity in SARS-CoV-2 infection by regulating CD4+ T cell recruitment

Project description:Understanding the host immune response to SARS-CoV-2 infection is critical for developing effective immunotherapeutic interventions. Using bulk RNA sequencing of lung tissue from mock-infected and mouse-adapted SARS-CoV-2 strain MA-10-infected mice, we identified CXCL9, CXCL10, and CXCL11 as among the most upregulated transcripts. Notably, their shared receptor, CXCR3, was also upregulated, suggesting activation of the CXCL9/10/11–CXCR3 axis in the lungs. Using spectral flow cytometry, we observed that the increased recruitment of CXCR3⁺ immune cells, particularly T cells, innate lymphoid cells (ILCs), and macrophages, correlated with milder disease outcome. Blocking CXCR3 signaling using monoclonal antibodies resulted in worsened disease, which was accompanied by reduced recruitment of T cells, ILCs, and macrophages, and a marked increase in neutrophil infiltration. Depletion of neutrophils using αLy6G antibodies in CXCR3-blocked mice alleviated disease severity, indicating that CXCR3 signaling mitigated neutrophil-driven pathology. CXCR3 blockade failed to exacerbate disease in RAG2⁻/⁻ mice, suggesting that CXCR3-mediated protection requires adaptive immune cells. Adoptive transfer of CD4⁺ T cells from wild type (WT), but not CXCR3⁻/⁻, mice conferred protection in RAG2⁻/⁻ mice. Together, our findings establish a protective role for CXCR3-recruited T cells blocking neutrophil infiltration in the lung, highlighting the mechanistic importance of the CXCL9/10/11–CXCR3 axis in protecting the lung from SARS-CoV-2 infection.

2026-06-08 | GSE309229 | GEO

Voluntary exercise suppresses tumor growth through exercise-directed recruitment and intratumoral infiltration of NK cells

2016-07-21 | GSE62628 | GEO

Glucocorticoids target the CXCL9/10-CXCR3 axis and confer protection against immune-mediated kidney injury

Project description:Glucocorticoids target the CXCL9/10-CXCR3 axis and confer protection against immune-mediated kidney injury

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Effect of minimum driving pressure guided individualized ventilation strategy on pulmonary function in elderly patients undergoing laparoscopic colorectal cancer surgery

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Mechanisms Driving Fasting-Induced Protection from Genotoxic Injury in the Small Intestine

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LSD1 inhibition promotes CD8+ T cells mediated anti-tumor immunity by MHC-I upregulation and enhanced infiltration of dendritic cells through IFNγ-CXCL9-CXCR3 axis

Project description:Poor infiltration of CD8+ cells and dysregulated MHC-I provide resistance to anti-cancer clinical therapies. This study aimed to uncover mechanisms of lysine-specific demethylase 1 (Kdm1a or LSD1) in antitumor immunity in Head and Neck Squamous cell carcinoma (HNSCC). LSD1 inhibition in syngeneic and chronic tobacco carcinogen-induced HNSCC mice recruited an activated dendritic cell (DCs), CD4+, and CD8+ T cells, enriched IFNγ in T cells, CXCL9 in DCs, and CXCR3 in T cells, evaluated by single cell RNA-seq analysis. Humanized HNSCC mice and TCGA data validate inverse correlation of Kdm1a with markers of DCs, CD8+ T cells, and their activating chemokines. LSD1 knockout or inhibitors in mouse HNSCC and co-culture showed MHC-I upregulation in tumors for efficient antigen presentation. Overall, LSD1 inhibition promoted DCs through IFNγ-CXCL9-CXCR3 axis and MHC-I upregulation in tumors to induce CD8+ T cell medicated antitumor immunity, which has implications for poorly immunogenic and immunotherapy-resistant cancers therapy.

2025-09-26 | GSE278349 | GEO

Therapeutic bacteria-trained NK cells confer long-term protection against cancer metastasis

Project description:We report that a single dose of therapeutic Salmonella, a prominent anti-tumor bacterial therapy, provides long-lasting protection against metastasis in mice by inducing trained NK cells. Integrated functional and multi-omics analyses revealed that Salmonella-trained NK (stNK) cells establish an enduring reprogrammed epigenome characterized by enhanced pro-survival signaling and immune effector functions, resulting in more potent IFN-gamma release and cytotoxicity upon secondary stimulation. We further showed that this training requires a transient pulse of IL-12 combined with sustained IL-18 signaling. Crucially, stNK cells significantly outperform conventional immune checkpoint therapies, including PD-1 and TIGIT blockade, in preventing metastasis, underscoring the unique immunological mechanisms in combating metastasis.

2026-05-28 | GSE333350 | GEO

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