Evidence map›Paper›PMID 41084279›Full record

ArticleClinical and translational medicine2025

Reprogrammed MDSCs promote Th1-dominant antitumour response via CD40 induced by autocrine TNF-α after combining cryo-thermal therapy with IL6 and IL17A neutralization.

Yuankai Hao, Shicheng Wang, Junjun Wang, Zelu Zhang, Yichen Yao, Ke Wang, Ping Liu, Lisa X Xu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
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  4. Article
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

8 authors.

Yuankai HaoMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Shicheng WangMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0003-3762-0046
Junjun WangMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Zelu ZhangMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Yichen YaoMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Ke WangMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Ping LiuMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0001-5209-9602
Lisa X XuMed-X Research Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.

Funding

National Key R&D Program of China 2020YFA0909000National Key R&D Program of China 2020YFA0909003National Key R&D Program of China 2023YFC2411400National Key R&D Program of China 2023YFC2411403
6 · The paper itself

Abstract

backgroundMounting evidence shows that myeloid-derived suppressor cells (MDSCs) reprogramming can significantly enhance the outcomes of immunotherapy. However, the therapeutic potential of targeting MDSCs alone is limited by persistent immunosuppressive cytokines and cellular crosstalk. In our previous study, we found that novel cryo-thermal therapy (CTT) can drive MDSCs maturation and induce CD4

methodsThe combination therapy was implemented in LLC1 tumor-bearing mice. We then observed its impacts on MDSCs maturation and Th1 differentiation and explored the related mechanisms by examining various aspects including the expression of CD40, the reactive oxygen species (ROS)-nuclear factor-kappa B (NF-κB) pathway, and the induction of tumor necrosis factor-α (TNF-α).

resultsIt was observed that the combination therapy increased the expression of CD40 on MDSCs through the ROS-NF-κB pathway-dependent TNF-α induction. This TNF-α-mediated CD40 upregulation facilitated Th1 polarization via CD40L engagement on CD4

conclusionOur research elucidated the methods and mechanisms of MDSCs reprogramming and offered a promising therapeutic strategy for patients with NSCLC and other types of cancer.

Indexed as

CD40 AntigensInterleukin-17Interleukin-6Interleukin-6 InhibitorsMyeloid-Derived Suppressor CellsTh1 CellsTumor Necrosis Factor-alphaAnimalsMiceMice, Inbred C57BLCD40 AntigensInterleukin-17Interleukin-6Interleukin-6 InhibitorsTumor Necrosis Factor-alphaCD40CD4‐positive T‐lymphocytesinterleukin‐17Ainterleukin‐6myeloid‐derived suppressor cellstumour necrosis factor‐alpha (TNF‐α)

Identifiers

PMID41084279
PMCPMC12518503

What Socratic holds

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LicenceCC BY
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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 Socratic graph.