Evidence map›Paper›PMID 34525267›Full record

ArticleImmunity, inflammation and disease2021

CCL2 produced by pancreatic ductal adenocarcinoma is essential for the accumulation and activation of monocytic myeloid-derived suppressor cells.

Haitao Gu, Wensheng Deng, Zhong Zheng, Ke Wu, Feng Sun

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  8. CAR-Macrophage Cell Therapy: A New Era of Hope for Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Review
  9. Article
  10. Inflammation, microbiota, and pancreatic cancer.Cancer cell international · 2025
    Review
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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

5 authors at 1 institution in 1 country.

Haitao GuDepartment of General Surgery, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Wensheng DengDepartment of General Surgery, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Zhong ZhengDepartment of Urology, School of Medicine, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Ke WuDepartment of Urology, School of Medicine, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0003-1151-3146
Feng SunDepartment of Urology, School of Medicine, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe development of pancreatic ductal adenocarcinoma (PDAC) is closely tied with the immune system. C-C motif chemokine ligands (CCL) were proved to lead to immune recruitment and training. Thus, we reckoned CCL2 to be the kernel of immune suppression in PDAC tissues.

methodsWe compared normal pancreatic tissues with PDAC tissues according to The Cancer Genome Atlas (TCGA) and clinical samples. Flow cytometry was used to identify M-MDSCs. We further demonstrated immune suppression of M-MDSCs according to proliferation rates of CD8

resultsWe found that CCL2 highly increased in PDAC tissues. CCL2 is positively related to CD33 and CD14, markers of monocytic myeloid-derived suppressor cells (M-MDSCs). We have demonstrated that CCL2 recruited M-MDSCs into PDAC tissues both in vitro and in vivo. M-MDSCs recruitment is accompanied by sustained immune suppression. Furthermore, we have found that M-MDSCs impeded T cell proliferation and produced high levels of ROS and Arginase, which can be enhanced by CCL2. Mechanistically, CCL2 stimulated M-MDSCs led to a significant upregulation of genes, a large part of which accumulated in the mitogen-activated protein kinase signaling pathway. Treatment of aloesin, MAPK signaling inhibitor, relieved the associated immunosuppressive phenotype induced by CCL2.

conclusionsOur study indicates that PDAC cells produced CCL2, which promoted localized M-MDSC recruitment and immune suppression, thereby promoting tumor progression.

Indexed as

AdenocarcinomaMyeloid-Derived Suppressor CellsPancreatic NeoplasmsCD8-Positive T-LymphocytesCells, CulturedChemokine CCL2HumansCCL2 protein, humanChemokine CCL2CCL2immune suppressionM-MDSCspancreatic ductal adenocarcinoma

Identifiers

PMID34525267
PMCPMC8589368
OpenAlexW3200330839

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.