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Oncolytic ORFV induces antitumor immunity

ABSTRACT: Oncolytic ORFV induces antitumor immunity

PROVIDER: PRJNA851624 | ENA |

REPOSITORIES: ENA

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Oncolytic ORFV induces antitumor immunity

Project description:To study the oncolytic effect of ORFV on tumors, we performed ORFV treatment (i.t.) in B16 engrafted tumors, changes of gene transcripts were detected

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Thymosin α1 reverses oncolytic adenovirus-induced M2 polarization of macrophages to improve antitumor immunity and therapeutic efficacy

Project description:Although oncolytic adenoviruses have been widely studied for their direct oncolytic activity and immunomodulatory role in cancer immunotherapy, the immunosuppressive feedback loop induced by oncolytic adenoviruses remains poorly studied. Here, we showed that type V adenovirus (ADV) induces the polarization of tumor-associated macrophages (TAMs) to the M2 phenotype and increases the infiltration of regulatory T cells (Tregs) in the tumor microenvironment (TME). By selectively compensating for these deficiencies, Tα1 reprogrammed “M2-like” TAMs toward an antitumoral phenotype, thereby reprogramming the TME into a state more beneficial for antitumor immunity. Moreover, ADVTα1 was constructed by harnessing the merits of all the components for the aforementioned combinatorial therapy. Both in vitro and in vivo data showed that both exogenously supplied and adenovirus-produced Tα1 orchestrate TAM reprogramming and enhance the antitumor efficacy of ADV via CD8+ T cells, showing promising prospects for clinical translation. Our findings provide inspiration for improving oncolytic adenovirus combination therapy and designing new oncolytic engineered adenoviruses.

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Thymosin α1 reverses oncolytic adenovirus-induced M2 polarization of macrophages to improve antitumor immunity and therapeutic efficacy

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m1A inhibition fuels oncolytic virus-elicited antitumor immunity via downregulating PD-L1 expression

Project description:RNA N1-methyladenosine methylation (m1A) modification is critical in regulating mRNA translation and thus protein synthesis, but the role of m1A modification in the occurrence, progression, and immunotherapy of head and neck squamous cell cancer (HNSCC) remains largely unknown. In Tgfbr1/Pten 2cKO mice, we found that the spontaneous neoplastic transformation of oral mucosa is accompanied by elevated levels of m1A modification. Analysis of m1A-associated genes identified TRMT61A as the key m1A writer associated with cancer progression, and poor prognosis. Mechanically, TRMT61A-induced tRNA-m1A modification promotes MYC protein synthesis and subsequent programmed death-ligand 1 (PD-L1) expression. In Tgfbr1/Pten 2cKO mice, RNA-m1A modification levels are also elevated in tumors that developed resistance to oncolytic herpes simplex virus (oHSV) treatment. Therapeutic inhibition of m1A modification sustains oncolytic virus-induced antitumor immunity and reduces tumor growth, providing a promising strategy for alleviating resistance to oHSV therapy. These findings indicate that m1A inhibition can prevent immune escape after oHSV therapy by reducing the expression of PD-L1. Our results provide a mutually reinforcing strategy for clinical combination immunotherapy.

2024-03-31 | GSE247024 | GEO

m1A inhibition fuels oncolytic virus-elicited antitumor immunity via downregulating PD-L1 expression

Project description:m1A inhibition fuels oncolytic virus-elicited antitumor immunity via downregulating PD-L1 expression

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A single local delivery of paclitaxel and nucleic acids via an immunoactive polymer eliminates solid tumors and induces systemic antitumor immunity

Project description:Despite recent advances in cancer therapy, hard-to-reach, unidentified tumors remain a significant clinical challenge. A promising approach is to treat locatable and accessible tumors locally and stimulate antitumor immunity in situ to exert systemic effects against distant tumors. We hypothesize that a local carrier of immunotherapeutics is critical to the effective activation of in-situ antitumor immunity. Here, we develop a polyethyleneimine derivative (2E’), which activates immune cells and co-delivers hydrophobic immunogenic cell death inducers and immunomodulatory nucleic acids/nucleotides. A single local administration of 2E’ or its combination with paclitaxel and PD-L1 siRNA or cyclic dinucleotide induces strong antitumor immunity, resulting in immediate regression of large established tumors, tumor-free survival, and the resistance to rechallenge and metastasis in different models. This study supports that effective in-situ induction of antitumor immunity can lead to systemic protection from distant and recurrent diseases, where 2E’ plays multiple roles as a simple and versatile carrier of immunotherapeutics.

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Suppression of antitumor immunity by the oncometabolite 2-hydroxyglutarate

Project description:Isocitrate dehydrogenase (IDH) mutations, a hallmark of gliomagenesis, result in the production of the oncometabolite R-2-hydroxyglutarate (R-2-HG) which is thought to promote tumorigenesis via DNA methylation. Here we identify an additional immunosuppressive activity of R-2-HG: Tumor cell-derived R-2-HG is taken up by T-cells where it induces a strong and immediate perturbation of calcium- and ATP-dependent signaling events, and polyamine biosynthesis. This results in a profound suppression of antigen-specific T-cell activation and effector cytokine production in experimental mouse and human systems. In a large cohort of WHO grade II and III gliomas, IDH1 mutant tumors display reduced infiltration by T-cells compared to IDH1 wildtype tumors. Spontaneous and induced mutation-specific antitumor immunity to syngeneic IDH1-mutant tumors in MHC-humanized mice is improved by isolated genetic ablation of the neomorphic enzymatic function of mutant IDH1. Taken together, these data attribute a novel, fundamentally non-tumor-cell-autonomous role of an oncometabolite in shaping the tumor immune microenvironment. We investigated the effects of exogenous R-2-HG on primary human T cells.

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SETDB1-TRIM28 complex suppresses antitumor immunity

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