Evidence map›Paper›PMID 41545307›Full record

ArticleJournal for immunotherapy of cancer2026

CD300ld blockade overcomes PMN-MDSC-mediated vaccine resistance in advanced tumors.

Xianglei Wang, Shiyao Xue, Yuwei Li, Miaomiao Yang, Haotian Yu, Mengyan Wang, Suxin Li, Zhigang Lu, Min Luo

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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Xianglei Wang *Institute of Pediatrics of Children's Hospital of Fudan University, Shanghai Key Laboratory of Medical Epigenetics, Shanghai Key Laboratory of Oncology Target Discovery and Antibody Drug Development, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0009-5357-4845
Shiyao Xue *Institute of Pediatrics of Children's Hospital of Fudan University, Shanghai Key Laboratory of Medical Epigenetics, Shanghai Key Laboratory of Oncology Target Discovery and Antibody Drug Development, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Yuwei Li *Institute of Pediatrics of Children's Hospital of Fudan University, Shanghai Key Laboratory of Medical Epigenetics, Shanghai Key Laboratory of Oncology Target Discovery and Antibody Drug Development, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China 20111510023@fudan.edu.cn zhiganglu@fudan.edu.cn luo_min@fudan.edu.cn.
Miaomiao YangInstitute of Pediatrics of Children's Hospital of Fudan University, Shanghai Key Laboratory of Medical Epigenetics, Shanghai Key Laboratory of Oncology Target Discovery and Antibody Drug Development, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Haotian YuInstitute of Pediatrics of Children's Hospital of Fudan University, Shanghai Key Laboratory of Medical Epigenetics, Shanghai Key Laboratory of Oncology Target Discovery and Antibody Drug Development, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Mengyan WangInstitute of Pediatrics of Children's Hospital of Fudan University, Shanghai Key Laboratory of Medical Epigenetics, Shanghai Key Laboratory of Oncology Target Discovery and Antibody Drug Development, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Suxin LiState Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Druggability of Biopharmaceuticals, Department of Pharmaceutics, China Pharmaceutical University, Nanjing, China.
Zhigang LuThe Fifth People's Hospital of Shanghai, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China 20111510023@fudan.edu.cn zhiganglu@fudan.edu.cn luo_min@fudan.edu.cn.
Min LuoInstitute of Pediatrics of Children's Hospital of Fudan University, Shanghai Key Laboratory of Medical Epigenetics, Shanghai Key Laboratory of Oncology Target Discovery and Antibody Drug Development, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China 20111510023@fudan.edu.cn zhiganglu@fudan.edu.cn luo_min@fudan.edu.cn.ORCID http://orcid.org/0000-0001-5732-4848

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhile cancer vaccines have demonstrated promising clinical potential, their therapeutic efficacy against advanced tumors remains suboptimal, highlighting the critical need to elucidate resistance mechanisms and develop targeted solutions. We previously developed a stimulator of interferon genes (STING)-activating PC7A nanovaccine that elicits strong antitumor efficacy in multiple tumor models. In this study, we systematically investigated the mechanisms mediating nanovaccine resistance and provided targeting approaches to overcome this therapeutic barrier.

methodsVaccine efficacy at early stage and advanced-stage tumors was investigated in the B16-OVA melanoma model and TC-1 human papillomavirus-induced cancer model, with tumor microenvironment being comprehensively analyzed by flow cytometry. In a vaccine-resistant tumor, elevated immunosuppressive activity of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) was assessed through multi-analysis including surface marker staining, reverse transcription-quantitative PCR, and functional T cell-suppression assay. To investigate the CD300ld blockade strategy, we employed CD300ld-knockout (KO) mice for genetic ablation, or recombinant protein capable of competitive inhibition for pharmacological intervention. For clinical relevance assessment, we tested different cancer vaccine formulations at late-stage tumors in humanized-CD3000ld mice.

resultsIn contrast to early stage vaccination, PC7A nanovaccine administration at the late tumor stage exhibited minimal therapeutic effects on tumor progression, while concurrently increasing PMN-MDSC infiltration and enhancing their immunosuppressive activity. KO of CD300ld, a critical immune suppressor on PMN-MDSCs, abolished both PMN-MDSC recruitment and their T-cell suppressive function, restoring the antitumor efficacy of PC7A vaccine in multiple advanced tumor models. Furthermore, in wild-type and CD300ld humanized mouse models, competitive blockade of CD300ld using recombinant extracellular domain proteins overcame resistance of advanced tumors to different cancer vaccine formulations.

conclusionOur results reveal that vaccination at the late tumor stage significantly augments the recruitment and immunosuppressive capacity of PMN-MDSCs, driving resistance of advanced tumors to cancer vaccines. The findings demonstrate PMN-MDSCs as critical mediators of vaccine resistance in advanced tumors and highlight modulation of PMN-MDSCs by CD300ld blockade as a promising strategy to enhance the therapeutic efficacy of cancer vaccines, particularly for patients with late-stage malignancies.

Indexed as

Cancer VaccinesMelanoma, ExperimentalMyeloid-Derived Suppressor CellsReceptors, ImmunologicAnimalsCell Line, TumorFemaleHumansMiceMice, Inbred C57BLMice, KnockoutNanovaccinesTumor MicroenvironmentCancer VaccinesNanovaccinesReceptors, Immunologicimmunosuppressionimmunotherapyneutrophilvaccine

Identifiers

PMID41545307
PMCPMC12815194

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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.