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Bexmarilimab activates human tumor-associated macrophages to support adaptive immune responses in interferon-poor immune microenvironments

ABSTRACT: Bexmarilimab activates human tumor-associated macrophages to support adaptive immune responses in interferon-poor immune microenvironments

PROVIDER: PRJNA922959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23051000.fastq.gz	Fastqsanger.gz
	SRR23051001.fastq.gz	Fastqsanger.gz
	SRR23051002.fastq.gz	Fastqsanger.gz
	SRR23051003.fastq.gz	Fastqsanger.gz
	SRR23051004.fastq.gz	Fastqsanger.gz

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Bexmarilimab activates human tumor-associated macrophages to support adaptive immune responses in interferon-poor immune microenvironments

Project description:Immune checkpoint inhibitors (ICI) show substantially greater efficacy in inflamed tumors characterized by preexisting T-cell infiltration and IFN signaling than in noninflamed “cold” tumors, which often remain immunotherapy resistant. The cancer immunotherapy bexmarilimab, which inhibits the scavenger receptor Clever-1 to release macrophage immunosuppression and activate adaptive immunity, has shown treatment benefit in subsets of patients with advanced solid malignancies. However, the mechanisms that determine bexmarilimab therapy outcome in individual patients are unknown. Here we characterized bexmarilimab response in ovarian cancer ascites macrophages ex vivo using single-cell RNA-sequencing and demonstrated increased IFN signaling and CXCL10 secretion following bexmarilimab treatment. We further showed that bexmarilimab was most efficacious in macrophages with low baseline IFN signaling, as chronic IFNγ priming abolished bexmarilimab-induced TNFα release. These results highlight an approach to target immunologically cold tumors and to increase the likelihood of their subsequent response to ICIs.

2023-10-30 | GSE222649 | GEO

Bexmarilimab Activates Human Tumor-Associated Macrophages to Support Adaptive Immune Responses in Interferon-Poor Immune Microenvironments.

Project description:Immune checkpoint inhibitors (ICI) show substantially greater efficacy in inflamed tumors characterized by preexisting T-cell infiltration and IFN signaling than in noninflamed "cold" tumors, which often remain immunotherapy resistant. The cancer immunotherapy bexmarilimab, which inhibits the scavenger receptor Clever-1 to release macrophage immunosuppression and activate adaptive immunity, has shown treatment benefit in subsets of patients with advanced solid malignancies. However, the mechanisms that determine bexmarilimab therapy outcome in individual patients are unknown. Here we characterized bexmarilimab response in ovarian cancer ascites macrophages ex vivo using single-cell RNA sequencing and demonstrated increased IFN signaling and CXCL10 secretion following bexmarilimab treatment. We further showed that bexmarilimab was most efficacious in macrophages with low baseline IFN signaling, as chronic IFNγ priming abolished bexmarilimab-induced TNFα release. These results highlight an approach to target immunologically cold tumors and to increase the likelihood of their subsequent response to ICIs.

| S-EPMC10762336 | biostudies-literature

Immune microenvironments differ in immune characteristics and outcome of glioblastoma multiforme

Project description:Immune microenvironments differ in immune characteristics and outcome of glioblastoma multiforme

| PRJNA505674 | ENA

Immune microenvironments differ in immune characteristics and outcome of glioblastoma multiforme

Project description:Understanding the interactions between tumors and the host immune system holds great promise to uncover biomarkers for targeted therapies, predict the prognosis of patients and guide clinical treatment. However, the immune signatures of glioblastoma multiforme (GBM) remain largely unstudied in terms of systematic analyses. We aimed to classify GBM samples according to immune-related genes and complement the existing immunotherapy system knowledge. In this study, we designed a strategy to identify 3 immune subtypes representing 3 different immune microenvironments (M1-M3) and associated with prognosis. The three subtypes were significantly different in terms of specific immune characteristics (immune cell subpopulations, immune responses, immune cells and checkpoint gene interactions). In additional, somatic alterations and methylation changes were identified that correlated with genes related to a worse prognosis subtype in the microenvironment. More importantly, in M3 (worst prognosis subtype) and M2 (best prognosis subtype), the interaction between immune cells and checkpoint genes was different, and this had an important effect on the prognosis. Finally, we used risk scores of immune cells and checkpoint genes to evaluate the prognosis of GBM patients and validated the results with 3 independent datasets. Disordered interactions between immune cells and checkpoint genes result in a change in the immune microenvironment and affects the prognosis of patients. We propose that a better understanding of the immune microenvironment of advanced cancers may provide new insights into immunotherapy.

2019-06-20 | GSE122586 | GEO

Subclonal cooperation drives metastasis through modulating local and systemic immune microenvironments

Project description:Subclonal cooperation drives metastasis through modulating local and systemic immune microenvironments

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Immunoediting instructs tumor metabolic reprogramming to support immune evasion

Project description:Immunoediting instructs tumor metabolic reprogramming to support immune evasion

| PRJNA899086 | ENA

Low neoantigen expression and poor T cell priming underlie early immune escape in cancer

Project description:Low neoantigen expression and poor T cell priming underlie early immune escape in cancer

2021-06-17 | MSV000087648 | MassIVE

Immunoediting instructs tumor metabolic reprogramming to support immune evasion [smartseq]

Project description:Immunoediting instructs tumor metabolic reprogramming to support immune evasion [smartseq]

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Immunoediting instructs tumor metabolic reprogramming to support immune evasion [ExomeSeq]

Project description:Immunoediting instructs tumor metabolic reprogramming to support immune evasion [ExomeSeq]

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Distinct immune microenvironments between primary and paired metastatic tumors in gastric cancer patients

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