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Cancer immunotherapy via synergistic co-activation of myeloid cells [scRNA-seq]

ABSTRACT: Cancer immunotherapy via synergistic co-activation of myeloid cells [scRNA-seq]

PROVIDER: PRJNA975171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24687449.fastq.gz	Fastqsanger.gz
	SRR24687450.fastq.gz	Fastqsanger.gz
	SRR24687451.fastq.gz	Fastqsanger.gz
	SRR24687452.fastq.gz	Fastqsanger.gz
	SRR24687453.fastq.gz	Fastqsanger.gz

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Cancer immunotherapy via synergistic co-activation of myeloid cells

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Project description:Myeloid cells coordinate T cell immune evasion in cancer yet are pliable and possess anti-tumor potential. Here, by co-targeting activation molecules we leverage the myeloid compartment as a therapeutic vulnerability in cancer. Myeloid cells in solid tumors expressed activation receptors including the pattern recognition receptor CLEC7A and the TNF receptor superfamily member CD40. In mouse models of checkpoint inhibitor-resistant pancreatic cancer, co-activation of CLEC7A, via systemic β-glucan therapy, and CD40, with agonist antibody treatment, eradicated established tumors and induced immunological memory. Anti-tumor activity was dependent on a cDC1 – T cell axis but did not require classical T cell cytotoxicity or blockade of checkpoint molecules. Rather, targeting CD40 drove T cell-derived IFNγ signaling which converged with CLEC7A activation to program distinct macrophage subsets to facilitate tumor responses. Thus, productive cancer immune surveillance can be invoked by co-activation of complementary myeloid signaling pathways.

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Cancer immunotherapy via synergistic co-activation of myeloid cells [scRNA-seq]

Project description:The goal of this study was to define the impact of beta-glucan (CLEC7A agonist), anti-CD40 (agonist) and the combination of beta-glucan and anti-CD40 on the intra-tumoral immune landscape of mouse orthotopic pancreatic tumors using single-cell RNA sequencing.

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Project description:Checkpoint immunotherapy unleashes T cell effector functions that control tumor growth, but can be undermined by myeloid cells that induce immunosuppression. TREM2 is a myeloid surface receptor that binds lipids and transmits intracellular signals through protein-tyrosine phosphorylation known to sustain microglial responses during Alzheimer’s disease. Intriguingly, TREM2 expression has recently been noted in tumor-infiltrating macrophages. We found that Trem2–/– mice are more resistant to growth of sarcoma, colorectal and mammary cancer cells than wild-type mice and are more responsive to anti-PD-1 immunotherapy. Furthermore, treatment with anti-TREM2 mAb curbed tumor growth and led to complete tumor regression when combined with anti-PD-1. scRNA-seq revealed that both constitutive TREM2 deficiency and anti-TREM2 are associated with relatively scant representation of MRC1+ and CX3CR1+ subsets in the macrophage tumor infiltrate, paralleled by expansion of subsets expressing immunostimulatory molecules. These changes were associated with improved T cell responses. TREM2 expression was evident in tumor macrophages in over 200 human cancer cases examined and inversely correlated with prolonged survival for two types of cancer. Thus, TREM2 is a promising target to modify tumor-infiltrating myeloid cells and effectively augment checkpoint immunotherapy.

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Cancer immunotherapy via synergistic co-activation of myeloid cells

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