Evidence map›Paper›PMID 35785030›Full record

ArticleJournal of immunology research2022

Targeting Inhibition of Accumulation and Function of Myeloid-Derived Suppressor Cells by Artemisinin via PI3K/AKT, mTOR, and MAPK Pathways Enhances Anti-PD-L1 Immunotherapy in Melanoma and Liver Tumors.

Mengqi Zhang, Lulu Wang, Wan Liu, Tian Wang, Francesco De Sanctis, Lifang Zhu, Guizhong Zhang, Jian Cheng, Qin Cao, Jingying Zhou and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% of its field
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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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  18. MDSC: a new potential breakthrough in CAR-T therapy for solid tumors.Cell communication and signaling : CCS · 2024
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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

15 authors at 6 institutions in 3 countries.

Mengqi ZhangSchool of Basic Medical Science, Jinzhou Medical University, Jinzhou 121000, China.
Lulu WangDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen 518036, China.
Wan LiuGuangdong Immune Cell Therapy Engineering and Technology Research Center, Center for Protein and Cell-Based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.
Tian WangDepartment of Medicine, Immunology Section, University of Verona, Verona, Italy.
Francesco De SanctisDepartment of Medicine, Immunology Section, University of Verona, Verona, Italy.
Lifang ZhuGuangdong Immune Cell Therapy Engineering and Technology Research Center, Center for Protein and Cell-Based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.
Guizhong ZhangGuangdong Immune Cell Therapy Engineering and Technology Research Center, Center for Protein and Cell-Based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.
Jian ChengSchool of Basic Medical Science, Jinzhou Medical University, Jinzhou 121000, China.
Qin CaoSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong.
Jingying ZhouSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong.
Aldo TagliabueGuangdong Immune Cell Therapy Engineering and Technology Research Center, Center for Protein and Cell-Based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.
Vincenzo BronteDepartment of Medicine, Immunology Section, University of Verona, Verona, Italy.ORCID https://orcid.org/0000-0002-3741-5141
Dehong YanGuangdong Immune Cell Therapy Engineering and Technology Research Center, Center for Protein and Cell-Based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.ORCID https://orcid.org/0000-0003-2258-4564
Xianchun WanGuangdong Immune Cell Therapy Engineering and Technology Research Center, Center for Protein and Cell-Based Drugs, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.ORCID https://orcid.org/0000-0003-3745-1860
Guang YuSchool of Basic Medical Science, Jinzhou Medical University, Jinzhou 121000, China.ORCID https://orcid.org/0000-0002-7872-0978
Chinese Academy of Sciences · CNUniversity of Verona · ITChinese University of Hong Kong · HKJinan University · CNJinzhou Medical University · CNShenzhen Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the remarkable success and efficacy of immune checkpoint blockade (ICB) therapy such as anti-PD-L1 antibody in treating cancers, myeloid-derived suppressor cells (MDSCs) that lead to the formation of the protumor immunosuppressive microenvironment are one of the major contributors to ICB resistance. Therefore, inhibition of MDSC accumulation and function is critical for further enhancing the therapeutic efficacy of anti-PD-L1 antibody in a majority of cancer patients. Artemisinin (ART), the most effective antimalarial drug with tumoricidal and immunoregulatory activities, is a potential option for cancer treatment. Although ART is reported to reduce MDSC levels in 4T1 breast tumor model and improve the therapeutic efficacy of anti-PD-L1 antibody in T cell lymphoma-bearing mice, how ART influences MDSC accumulation, function, and molecular pathways as well as MDSC-mediated anti-PD-L1 resistance in melanoma or liver tumors remains unknown. Here, we reported that ART blocks the accumulation and function of MDSCs by polarizing M2-like tumor-promoting phenotype towards M1-like antitumor one. This switch is regulated via PI3K/AKT, mTOR, and MAPK signaling pathways. Targeting MDSCs by ART could significantly reduce tumor growth in various mouse models. More importantly, the ART therapy remarkably enhanced the efficacy of anti-PD-L1 immunotherapy in tumor-bearing mice through promoting antitumor T cell infiltration and proliferation. These findings indicate that ART controls the functional polarization of MDSCs and targeting MDSCs by ART provides a novel therapeutic strategy to enhance anti-PD-L1 cancer immunotherapy.

Indexed as

ArtemisininsLiver NeoplasmsMelanomaMyeloid-Derived Suppressor CellsAnimalsB7-H1 AntigenImmunologic FactorsImmunotherapyMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTumor MicroenvironmentArtemisininsB7-H1 AntigenImmunologic FactorsmTOR protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID35785030
PMCPMC9247850
OpenAlexW4283315160

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.