Evidence map›Paper›PMID 41663428›Full record

ArticleNature communications2026

Triple targeting of STING, TGF-β, and PD-L1 boosts CXCL16-CXCR6 signaling for potent antitumor response.

Ming Yi, Tianye Li, Yinhui Gu, Mengke Niu, Dixuan Xue, Shengtao Hu, Yuze Wu, Bin Zhao, Di Zhang, Yingkang Ma and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. From M7824 to SHR-1701: lessons for dual PD-L1/TGF-β targeting.Journal for immunotherapy of cancer · 2026
    Article
  9. Interstitial lung disease and the STING pathway.The Journal of clinical investigation · 2026
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Targeting innate immunity to overcome immune evasion in HPV-associated cancers.Frontiers in cellular and infection microbiology · 2026
    Review
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

19 authors.

Ming Yi *Department of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China. mingyi2022@zju.edu.cn.ORCID http://orcid.org/0000-0001-5243-6613
Tianye Li *Department of Gynecology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, PR China.
Yinhui Gu *Zhejiang Key Laboratory of Smart Biomaterials and Key Laboratory of Biomass Chemical Engineering of Ministry of Education, College of Chemical and Biological Engineering, Zhejiang University, Hangzhou, PR China.
Mengke NiuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.ORCID http://orcid.org/0009-0004-4029-8208
Dixuan XueDepartment of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Shengtao HuDepartment of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Yuze WuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Bin ZhaoDepartment of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Di ZhangDepartment of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Yingkang MaDepartment of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Minjun ZhangDepartment of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China.
Jing ZhangWuhan YZY Biopharma Co., Ltd, Wuhan, PR China.
Yongxiang YanWuhan YZY Biopharma Co., Ltd, Wuhan, PR China.
Pengfei ZhouWuhan YZY Biopharma Co., Ltd, Wuhan, PR China.
Xiaojun ZhangCancer Center, Shanxi Bethune Hospital, Shanxi Academy of Medical Science, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, PR China.
Zhuxian ZhouZhejiang Key Laboratory of Smart Biomaterials and Key Laboratory of Biomass Chemical Engineering of Ministry of Education, College of Chemical and Biological Engineering, Zhejiang University, Hangzhou, PR China.ORCID http://orcid.org/0000-0002-7104-9915
Qian ChuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China. qianchu@tjh.tjmu.edu.cn.ORCID http://orcid.org/0000-0001-8192-7630
Kongming WuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China. kmwu@tjh.tjmu.edu.cn.ORCID http://orcid.org/0000-0003-2499-1032
Zhijun DaiDepartment of Breast Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, PR China. dzj0911@zju.edu.cn.ORCID http://orcid.org/0000-0001-5209-8626

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82373281National Natural Science Foundation of China (National Science Foundation of China) 82403929National Natural Science Foundation of China (National Science Foundation of China) 82573178Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LQ24H160007
6 · The paper itself

Abstract

Antibodies targeting TGF-β and PD-L1 initially showed promise as second-generation PD-L1 agents. However, consecutive trial failures have limited their clinical success. Our study reveals that the efficacy of the TGF-β×PD-L1 bispecific antibody (BsAb) is compromised by insufficient activation of innate immune responses. To address this, we combine STING agonists with the BsAb, significantly enhancing tumor suppression beyond that achieved with standard STING agonist plus anti-PD-L1 combinations in preclinical models. Unexpectedly, even STING agonist monotherapy is improved by TGF-β blockade, suggesting that TGF-β suppresses STING-driven immune activation. We find that this synergy is mediated by the CXCL16-CXCR6 axis, where STING activation and TGF-β blockade promote CXCL16 expression in macrophages and dendritic cells, recruiting and sustaining cytotoxic CXCR6

Indexed as

B7-H1 AntigenChemokine CXCL16Membrane ProteinsReceptors, CXCR6Transforming Growth Factor betaAnimalsCell Line, TumorcGAS-STING Signaling PathwayDendritic CellsFemaleHumansMacrophagesMiceMice, Inbred C57BLSignal TransductionSTING ProteinB7-H1 AntigenCd274 protein, mouseChemokine CXCL16Cxcl16 protein, mouseCxcr6 protein, mouseMembrane ProteinsReceptors, CXCR6Sting1 protein, mouseSTING ProteinTransforming Growth Factor beta

Identifiers

PMID41663428
PMCPMC12886787

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.