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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

ABSTRACT: Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

PROVIDER: PRJNA578135 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10302400.fastq.gz	Fastqsanger.gz
	SRR10302401.fastq.gz	Fastqsanger.gz
	SRR10302402.fastq.gz	Fastqsanger.gz
	SRR10302403.fastq.gz	Fastqsanger.gz
	SRR10302404.fastq.gz	Fastqsanger.gz

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (scRNA-seq dataset: SZ11)

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ3)

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ3)

Project description:In this study we searched for primary regulators of cancer-inhibitory inflammation using murine tumors of immune-dependent progressive or regressive fates linked to antagonistic inflammatory tumor microenvironments

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (scRNA-seq dataset: SZ11)

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Antagonistic Inflammatory Phenotypes Dictate Tumor Fate and Response to Immune Checkpoint Blockade.

Project description:Inflammation can support or restrain cancer progression and the response to therapy. Here, we searched for primary regulators of cancer-inhibitory inflammation through deep profiling of inflammatory tumor microenvironments (TMEs) linked to immune-dependent control in mice. We found that early intratumoral accumulation of interferon gamma (IFN-γ)-producing natural killer (NK) cells induced a profound remodeling of the TME and unleashed cytotoxic T cell (CTL)-mediated tumor eradication. Mechanistically, tumor-derived prostaglandin E2 (PGE2) acted selectively on EP2 and EP4 receptors on NK cells, hampered the TME switch, and enabled immune evasion. Analysis of patient datasets across human cancers revealed distinct inflammatory TME phenotypes resembling those associated with cancer immune control versus escape in mice. This allowed us to generate a gene-expression signature that integrated opposing inflammatory factors and predicted patient survival and response to immune checkpoint blockade. Our findings identify features of the tumor inflammatory milieu associated with immune control of cancer and establish a strategy to predict immunotherapy outcomes.

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

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

2020-11-20 | GSE139047 | GEO

Antibody-lectin chimeras for glyco-immune checkpoint blockade

Project description:Despite the curative potential of checkpoint blockade immunotherapy, most patients remain unresponsive to existing treatments. Glyco-immune checkpoints – interactions of cell-surface glycans with lectin, or glycan-binding, immunoreceptors – have emerged as prominent mechanisms of immune evasion and therapeutic resistance in cancer. Here, we describe antibody-lectin chimeras (AbLecs), a modular platform for glyco-immune checkpoint blockade. AbLecs are bispecific antibody-like molecules comprising a cell-targeting antibody domain and a lectin “decoy receptor” domain that directly binds glycans and blocks their ability to engage inhibitory lectin receptors. AbLecs potentiate anticancer immune responses including phagocytosis and cytotoxicity, outperforming most existing therapies and combinations tested. By targeting a distinct axis of immunological regulation, AbLecs synergize with blockade of established immune checkpoints. AbLecs can be readily designed to target numerous tumor and immune cell subsets as well as glyco-immune checkpoints, and therefore represent a new modality for cancer immunotherapy.

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Tumour mtDNA mutations drive aerobic glycolysis to enhance checkpoint blockade

Project description:Mitochondrial DNA (mtDNA) encodes essential machinery for respiration and metabolic homeostasis but is paradoxically among the most common targets of somatic mutations in the cancer genome, with truncating mutations in complex I genes being over-represented1 . While mtDNA mutations have been associated with both improved and worsened prognoses in several cancer lineages1–3, whether these mutations are drivers, or exert any functional effect on tumour biology remains controversial. Here we discover that complex I-encoding mtDNA mutations are sufficient to remodel the tumour immune landscape and therapeutic resistance to immune checkpoint blockade. Using mtDNA base editing technology we engineered recurrent truncating mutations in the mtDNA-encoded complex I gene, Mt-Nd5, into murine models of melanoma. Mechanistically, these mutations promoted utilisation of pyruvate as a terminal electron acceptor and increased glycolytic flux driven by an over-reduced NAD pool and NADH shuttling between GAPDH and MDH1, mediating a Warburg-like metabolic shift. In turn, without modifying tumour growth, this altered cancer cell-intrinsic metabolism reshaped the tumour microenvironment of mouse and human cancer in a mutation load-dependent fashion, encouraging an anti-tumour immune response. This subsequently sensitises both mouse and human cancers with high mtDNA mutant heteroplasmy to immune checkpoint blockade. Strikingly, patient lesions bearing >50% mtDNA mutation load demonstrated a >2.5-fold improved response rate to checkpoint inhibitor blockade. Taken together these data nominate mtDNA mutations as functional regulators of cancer metabolism and tumour biology, with potential for therapeutic exploitation and treatment stratification.

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