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STING activation improves T-cell-engaging immunotherapy of acute myeloid leukemia

ABSTRACT: STING activation improves T-cell-engaging immunotherapy of acute myeloid leukemia

PROVIDER: PRJNA1065460 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27585737_1.fastq.gz	Fastqsanger.gz
	SRR27585737_2.fastq.gz	Fastqsanger.gz

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STING activation improves T-cell-engaging immunotherapy of acute myeloid leukemia

Project description:T-cell recruiting bispecific antibodies (BsAbs) are in clinical development for relapsed/refractory acute myeloid leukemia (AML). Despite promising response rates, early clinical trials have failed to demonstrate durable responses. Here we investigated whether activation of the innate immune system through stimulator of interferon genes (STING) can enhance target-cell killing by a BsAb targeting CD33 (CD33 BiTE® molecule). Indeed, we show that cytotoxicity against AML mediated by the CD33 BiTE molecule AMG 330 can be greatly enhanced when combined with the STING agonist 2',3'-cyclic GMP–AMP (cGAMP). We used invitro cytotoxicity assays, immunoblotting, transcriptomic analyses, and extensive CRISPR–Cas9 knockout experiments to investigate the enhancing effect of cGAMP on the cytotoxicity of AMG330 against AML. Mechanistically, activated T cells prime target AML cells to STING activation through their effector cytokines interferon-gamma (IFNγ) and tumor necrosis factor (TNF), leading to increased production of typeI interferons and induction of interferon-stimulated genes. This feeds back to the T cells, leading to a further increase in effector cytokines and an overall cytotoxic T-cell phenotype, contributing to the beneficial effect of cGAMP in enhancing AMG330-mediated lysis. As such, we establish a key role for IFNγ in AMG 330-mediated cytotoxicity against AML cells, as well as in rendering AML cells responsive to STING agonism. Here, we propose to improve the efficacy of CD33-targeting BsAbs by combining them with a STING agonist.

2025-02-01 | GSE253398 | GEO

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Autophagy engaging and non-engaging hematopoietic stem cells

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The effect of myeloid STING knockout on gene expression in colitic mice

Project description:Myeloid-derived STING has been recognized to play a vital role in mediating the development of colitis. We here report that myeloid-specific knockout of STING in adult mice ameliorates DSS-induced acute colitis through inhibiting macrophage maturation, reducing DC cell activation, and suppressing pro-inflammatory Th1 and Th17 cells.

2024-08-14 | GSE252100 | GEO

The effect of myeloid STING knockout after tumor formation on gene expression in AOM/DSS-induced CAC mice

Project description:Myeloid-derived STING has been recognized to play a vital role in mediating the development of colitis-associated carcinoma (CAC). We here report that myeloid-specific knockout of STING after tumor formation enhanced tumor growth by modifying the tumor microenvironment to a more immunologically inactive state. Pathways related to antigen presentation, macrophage and DC activation, T cell chemotaxis and activation, T cell-mediated cytotoxicity and other immune responses to tumor cells were all inhibited by lateral myeloid STING kncckout after tumor formation.

2024-08-14 | GSE252099 | GEO

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C9orf72 in myeloid cells suppresses STING-induced inflammation

Project description:In this study we report that loss of C9orf72 expression in myeloid cells drives STING/type I interferon mediated autoimmunity and enhanced tumor immunity in mice. Additionally, we show that the immunophenotypic signature identified in C9orf72-/- mice is present in blood derived macrophages, whole blood and autopsy brain tissue from C9orf72 repeat expansion ALS/FTD patients.

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