Evidence map›Paper›PMID 42805762›Full record

ArticleJournal for immunotherapy of cancer2026

IL-23-engineered oncolytic vaccinia virus enhances pancreatic cancer control through inflammasome-driven Th17-skewed CD4

Yu Guo, Meng Wang, Yujing Xuan, Lvla Pan, Wenyi Yan, Jisiyu Cheng, Yang Yu, Xiangyu Wang, Lihua Xu, Xianlei Sun and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Yu Guo *Sino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.
Meng Wang *Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yujing XuanSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.
Lvla PanSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.
Wenyi YanSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.ORCID http://orcid.org/0000-0002-6641-667X
Jisiyu ChengShanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yang YuShanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Xiangyu WangShanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Lihua XuSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.
Xianlei SunSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.
Ruxia HanSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.
Lingling SiSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China.
Yaohe WangCentre for Biomarkers and Biotherapeutics, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0003-2367-6313
Sirui LiShanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China wangpengju@zzu.edu.cn sirui.li@sibcb.ac.cn.
Pengju WangSino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, State Key Laboratory of Metabolic Dysregulation and Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, School of Basic Medical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou, China wangpengju@zzu.edu.cn sirui.li@sibcb.ac.cn.ORCID http://orcid.org/0000-0002-1881-3902

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOncolytic viruses represent a promising immunotherapeutic strategy for converting pancreatic and other immunologically cold tumors. While their ability to stimulate innate immune signaling and promote antitumor immunity is established, mechanisms enabling durable adaptive responses remain poorly defined.

methodsWe used CRISPR-Cas9-based homologous recombination to generate a thymidine kinase (TK) and B2R double-deleted backbone virus, VV∆TK∆B2R (VV-DD). On this backbone, we engineered VV∆TKmp40∆B2Rmp19 (VV-DDIL23), which expresses the p40 and p19 subunits of interleukin-23 (IL-23) separately to mimic natural heterodimer assembly. Its antitumor efficacy was evaluated in immunosuppressive pancreatic ductal adenocarcinoma models and compared with a single-chain IL-23 fusion construct (VV-DDIL23F). In parallel, unbiased single-cell RNA sequencing was employed to systematically dissect the immune mechanisms underlying the potent antitumor activity of VV-DDIL23.

resultsVV-DDIL23 exhibited potent antitumor efficacy and significantly outperformed VV-DDIL23F. Single-cell RNA sequencing revealed that VV-DDIL23 enhanced antigen processing and presentation in macrophages, characterized by elevated major histocompatibility complex-II expression, upregulation of co-stimulatory molecules, and production of cytokines including interferon-I and IL-1β. This was accompanied by the emergence of a distinct population of tumor-infiltrating CD4

conclusionThis work reveals a previously unrecognized pathway linking innate viral recognition by macrophages to CD4

Indexed as

Carcinoma, Pancreatic DuctalCD4-Positive T-LymphocytesInflammasomesInterleukin-23Oncolytic VirotherapyOncolytic VirusesPancreatic NeoplasmsTh17 CellsVaccinia virusAnimalsCell Line, TumorFemaleHumansMiceInflammasomesInterleukin-23Gene therapyImmunotherapyIntratumoralOncolytic virus

Identifiers

PMID42805762
PMCPMC13630030

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.