Evidence map›Paper›PMID 41629977›Full record

ArticleJournal of nanobiotechnology2026

Tumor-activated dual metabolic nanomodulator turns over tolerogenic tumor control and unleashes systemic immune responses.

Xiaorong Kou, Xue Wu, Tao He, Liping Bai, Xinchao Li, Rui Luo, Yangsong Xu, Yixi Wang, Meiling Shen, Changyang Gong and 1 more

Abstract read
In one paragraph

Article in Journal of nanobiotechnology, 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.

Xiaorong Kou *Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Xue Wu *Department of Ophthalmology, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Tao HeDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Liping BaiDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Xinchao LiDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Rui LuoDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Yangsong XuDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Yixi WangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Meiling ShenDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Changyang GongDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China. chygong14@163.com.
Qinjie WuDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China. cellwqj@163.com.

Funding

National Key Research and Development Program of China 2023YFB3810004National Natural Science Foundation of China 82372123West China Hospital, Sichuan University ZYYC23004
6 · The paper itself

Abstract

Temporary amelioration of immunosuppression following extrinsic stress-induced immunogenic signal release provides opportunities for immunotherapy improvement. However, therapeutics that fail to translate local stimulatory clues into ongoing systemic antitumor responses would in turn hijack the alleviated immune status toward tolerance, instead of immunity. Here, we constructed a tumor-activated precise dual-metabolic nanomodulator (RAISE) that induced extensive tumor cell death while supporting DCs functions, thus synergistically turning over tolerogenic tumor control and skewing an antitumor immunity. Sequentially responsive to tumor-overexpressing enzymes and high intracellular GSH, RAISE disintegrated in a self-destructive manner, which facilitated drug release and produced immunogenic tumor cell death associated with immunosuppression relief. Then, the regression of tolerogenic metabolism by RAISE replenished intratumoral CD103

Indexed as

Immune ToleranceNeoplasmsAnimalsCell Line, TumorDendritic CellsFemaleHumansImmunotherapyIndoleamine-Pyrrole 2,3,-DioxygenaseLymphocyte ActivationMiceMice, Inbred C57BLT-LymphocytesIndoleamine-Pyrrole 2,3,-DioxygenaseImmune memoryImmunogenic cell deathImmunosuppression ameliorationMetabolic nanomodulatorTumor immunotherapy

Identifiers

PMID41629977
PMCPMC12955122

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.