Evidence map›Paper›PMID 25341727›Full record

ArticleJournal of leukocyte biology2015

Dopamine inhibits the function of Gr-1+CD115+ myeloid-derived suppressor cells through D1-like receptors and enhances anti-tumor immunity.

Jin Wu, Ruihua Zhang, Ning Tang, Zizhen Gong, Jiefei Zhou, Yingwei Chen, Kang Chen, Wei Cai

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

34 citing papers in PubMed, 45 citations in OpenAlex.

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  11. Cancer and neurotransmitter receptors.Chinese medical journal · 2025
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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

8 authors at 3 institutions in 2 countries.

Jin WuShanghai Institute for Pediatric Research and wujin51@yahoo.com caiw1978@163.com.
Ruihua Zhang
Ning TangShanghai Institute for Pediatric Research and.
Zizhen GongShanghai Institute for Pediatric Research and.
Jiefei ZhouShanghai Institute for Pediatric Research and.
Yingwei ChenShanghai Institute for Pediatric Research and Department of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China;
Kang ChenDepartments of Obstetrics and Gynecology, Immunology and Microbiology, Oncology, Wayne State University, Detroit, Michigan, USA; Perinatology Research Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, U.S. National Institutes of Health, Detroit, Michigan, USA; Tumor Biology and Microenvironment Program, Barbara Ann Karmanos Cancer Institute, Detroit, Michigan, USA; and Mucosal Immunology Studies Team, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, Bethesda, Maryland, USA.
Wei CaiShanghai Institute for Pediatric Research and wujin51@yahoo.com caiw1978@163.com.
Shanghai Institute of Nutrition and Health · CNEunice Kennedy Shriver National Institute of Child Health and Human Development · USIcahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MDSCs accumulate in tumor-bearing animals and cancer patients and are a major factor responsible for cancer-induced immunosuppression that limits effective cancer immunotherapy. Strategies aimed at effectively inhibiting the function of MDSCs are expected to enhance host anti-tumor immunity and improve cancer immunotherapy significantly. The neurotransmitter DA has been found to have anti-cancer activity, but the underlying mechanism is poorly understood. In this study, we sought to investigate the therapeutic mechanism and efficacy of DA on the inhibition of cancer development via the regulation of MDSC functions. The regulation of the suppressive function of Gr-1(+)CD115(+) MDSCs by DA was determined by use of murine syngeneic LLC and B16 graft models treated with DA in vivo, as well as Gr-1(+)CD115(+) MDSCs isolated from these model treated with DA ex vivo. Here, we show that Gr-1(+)CD115(+) monocytic MDSCs express D1-like DA receptors. DA dramatically attenuated the inhibitory function of tumor-induced monocytic MDSCs on T cell proliferation and IFN-γ production via D1-like DA receptors and retarded tumor growth. DA and other D1 receptor agonists inhibited IFN-γ-induced NO production by MDSCs from tumor-bearing mice and cancer patients. Decreased NO production was, in part, mediated via the suppression of p-ERK and p-JNK. In conclusion, the neurotransmitter DA potently inhibits the suppressive function of MDSC and enhances anti-tumor immunity. Our finding provides a mechanistic basis for the use of DA or D1-like receptor agonists to overcome tumor-induced immunosuppression in cancer immunotherapy.

Indexed as

AnimalsDopamineFlow CytometryHumansImmune ToleranceImmunoblottingLymphocyte ActivationMiceMice, Inbred C57BLMyeloid CellsNeoplasms, ExperimentalReceptors, Dopamine D1Reverse Transcriptase Polymerase Chain ReactionDopamineReceptors, Dopamine D1cancerimmune suppressioniNOSMDSCneurotransmitternitric oxide

Identifiers

PMID25341727
PMCPMC4377827
OpenAlexW2013296333

What OpenQuestion holds

Textmetadata
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.