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Rejuvenating endogenous antitumor immunity via a chimeric receptor-engineered oncolytic virus targeting tumor-associated macrophages

GSE272424 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/08/07 Platform GPL30215
Summary
Immunosuppressive tumor-associated macrophages (TAMs) create a barrier to effective antitumor immunity and promote therapeutic resistance. Reeducating TAMs to enhance their antitumor capabilities through phenotypic remodeling remains challenging. Here, we report a modular oncolytic herpesvirus platform, engineered with a PD-L1–specific chimeric receptor integrated into the viral envelope protein (CAR-oHSV). This design endows the virus with dual tropism, enabling it to target both tumor cells and TAMs within the tumor microenvironment. In virus-resistant tumor models, CAR-oHSV preferentially targets PD-L1⁺ TAMs and triggers a STING-dependent reprogramming into a CXCL9⁺ phenotype, enhancing their tumor antigen cross-presentation capability and inducing an endogenous antitumor T cell response. Furthermore, this platform can synergize with adoptive T cell therapy and immune checkpoint blockade therapy to overcome immunotherapy resistance. Collectively, our findings define a precision-oncolytic platform that dismantles TAM-mediated immunosuppression while amplifying adaptive immunity, offering a promising translational avenue for cancer immunotherapy.
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Direct links to NCBI, no account and no request form: the whole study as GSE272424_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1136852 and SRA study SRP520514. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, each sampled once — no replicated groups

Read from 6 sample titles: 6 distinct titles with little repetition. Check it against the sample list below before relying on it.

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