Evidence map›Paper›PMID 41926649›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Copper Depletion Nanoparticles Potentiate Cancer Immunotherapy by Avoiding Innate and Adaptive Immune Resistance.

Zaigang Zhou, Ke Li, Xuelan Li, Lei Yi, Zhengxiang Wang, Huan Ding, Sheng Wu, Feiyu Liu, Yuan Li, Rui Cheng and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

11 authors.

Zaigang ZhouZhejiang Key Laboratory of Ophthalmic Drug Discovery and Medical Device Research, Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Ke LiZhejiang Key Laboratory of Ophthalmic Drug Discovery and Medical Device Research, Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xuelan LiDepartment of Clinical Nursing, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lei YiDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhengxiang WangZhejiang Key Laboratory of Ophthalmic Drug Discovery and Medical Device Research, Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Huan DingZhejiang Key Laboratory of Ophthalmic Drug Discovery and Medical Device Research, Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Sheng WuZhejiang Key Laboratory of Ophthalmic Drug Discovery and Medical Device Research, Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Feiyu LiuZhejiang Key Laboratory of Ophthalmic Drug Discovery and Medical Device Research, Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yuan LiDepartment of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Rui ChengDepartment of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Jianliang ShenZhejiang Key Laboratory of Ophthalmic Drug Discovery and Medical Device Research, Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.ORCID https://orcid.org/0000-0003-4351-4872

Funding

Fundamental Research Funds for the Central Universities of the Central South University 2025ZZTS0291National Natural Science Foundation of China 22377093：22477097：82172878National Natural Science Foundation of China 82373435
6 · The paper itself

Abstract

Currently, cluster of differentiation 47 (CD47) and programmed death ligand 1 (PD-L1) targeted bispecific antibodies have been widely studied in clinical trials to overcome innate and adaptive immune resistance simultaneously. However, the excessive immune-related adverse events caused by the on-target off-tumor immune-toxicity cast a shadow over their future clinical usage. Thus, how to safely, effectively, and selectively regulate CD47 and PD-L1 in tumors at the same time is still a difficult issue to solve. Here, we developed a mitochondria-targeted copper-withdrawal nanoparticle CYN-CDA@Alb to more efficaciously depress CD47 and PD-L1 expression (only 1/50 dosage of common copper chelators), on account of the depression of mitochondria/Adenosine 5'-monophosphate-activated protein kinase (AMPK)/c-MYC signal pathway. By doing this, CYN-CDA@Alb reverses immune resistance by increasing T cell killing capacity and macrophage phagocytosis ability to tumor cells, leading to the following depressed tumor metastasis and slowed tumor growth. Moreover, CYN-CDA@Alb also avoids the usually increased innate and adaptive immune resistance after radiotherapy by depressing CD47 and PD-L1. Our findings altogether suggest the potential usage of copper ion-depleting nanoparticles as substitutes for CD47/PD-L1 bispecific antibodies to simultaneously overcome innate and adaptive immune-resistance.

Indexed as

Adaptive ImmunityCopperImmunity, InnateImmunotherapyNanoparticlesNeoplasmsAnimalsB7-H1 AntigenCD47 AntigenFemaleHumansMiceB7-H1 AntigenCD47 AntigenCoppercluster of differentiation 47copper depletion nanoparticlesimmune resistancemitochondriaprogrammed death ligand 1

Identifiers

PMID41926649
PMCPMC13252637

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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.