Evidence map›Paper›PMID 31145286›Full record

ArticleMedicine2019

CD4+CD25+Foxp3+ regulatory T cells suppress NKG2D-mediated NK cell cytotoxicity in peripheral blood.

Xu Geng, Ming Li, Bin Cui, Chao Lu, Xiaowen Liu, Peng Zhang, Bin Liu, Chunyan Ma, Yajuan Shen, Zhiming Lu

Open access · goldAbstract read
In one paragraph

Article in Medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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  8. Immunomodulation for Tissue Repair and Regeneration.Tissue engineering and regenerative medicine · 2023
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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

10 authors at 1 institution in 2 countries.

Xu GengDepartment of Clinical Laboratory.
Ming LiDepartment of Clinical Laboratory.
Bin CuiDepartment of Central Laboratory.
Chao LuDepartment of Clinical Laboratory.
Xiaowen LiuDepartment of Central Laboratory.
Peng ZhangDepartment of Liver Transplantation and Hepatobiliary Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, PR China.
Bin LiuDepartment of Central Laboratory.
Chunyan MaDepartment of Central Laboratory.
Yajuan ShenDepartment of Clinical Laboratory.
Zhiming LuDepartment of Clinical Laboratory.
Apple (Israel) · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStudies have shown that CD4CD25Foxp3Treg cells suppress NKG2D expression on NK cells via a cell contact-dependent mechanism and increased TGF-β and IL-10 production in some cancer models. We herein aimed to explore whether CD4CD25Foxp3Tregs suppress NKG2D-mediated NK cell cytotoxicity in peripheral blood and elucidate the exact mechanism underlying this phenomenon.

methodsTo explore the function of NKG2D, NK cell cultures were treated with an NKG2D-blocking antibody to block these receptors. Additionally, TGF-β- and IL-10-blocking antibodies were added to NK and CD4CD25Foxp3Treg cell cocultures to evaluate whether the latter cells suppress NKG2D expression of NK cells via increasing the production of TGF-β and IL-10. The expression of NKG2D on NK cells was detected by 3-color flow cytometry, and NK cell activity was assessed by 3 assays: a nonradioactive cytotoxicity assay, an ELISA measuring IFN-γ production and a flow cytometry assay to evaluate CD107a expression.

resultsBlocking NKG2D decreased NK cell cytotoxicity, IFN-γ production and CD107a expression. Moreover, blocking TGF-β and IL-10 substantially increased the NKG2D expression in NK and CD4CD25Foxp3Treg cell cocultures. Similarly, blocking TGF-β and IL-10 enhanced NK cell cytotoxicity, IFN-γ production and CD107a expression; Transwell insert assays also revealed increased IFN-γ production and CD107a and NKG2D expression.

conclusionCD4CD25Foxp3Tregs suppress NKG2D-mediated NK cell cytotoxicity in peripheral blood via a cell contact-dependent mechanism and increased TGF-β and IL-10 production.

Indexed as

AnimalsCytotoxicity, ImmunologicForkhead Transcription FactorsHumansInterleukin-2 Receptor alpha SubunitKiller Cells, NaturalLymphocyte ActivationMiceNK Cell Lectin-Like Receptor Subfamily KT-Lymphocytes, RegulatoryForkhead Transcription FactorsInterleukin-2 Receptor alpha SubunitNK Cell Lectin-Like Receptor Subfamily K

Identifiers

PMID31145286
PMCPMC6708973
OpenAlexW2978869678

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.