Evidence map›Paper›PMID 29909746›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2019

Trophoblast-Derived CXCL16 Decreased Granzyme B Production of Decidual γδ T Cells and Promoted Bcl-xL Expression of Trophoblasts.

Deng-Xuan Fan, Wen-Jie Zhou, Li-Ping Jin, Ming-Qing Li, Xiang-Hong Xu, Cong-Jian Xu

Open access · bronzeAbstract read
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Chemokines in Pregnancy.Biomolecules · 2025
    Review
  2. Review
  3. Article
  4. Review
  5. Review
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  7. Regulation and Function of Chemokines at the Maternal-Fetal Interface.Frontiers in cell and developmental biology · 2022
    Review
  8. Article
  9. 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

6 authors at 3 institutions in 1 country.

Deng-Xuan Fan1 Obstetrics and Gynecology Hospital, Fudan University, Shanghai, People's Republic of China.
Wen-Jie Zhou1 Obstetrics and Gynecology Hospital, Fudan University, Shanghai, People's Republic of China.
Li-Ping Jin2 Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China.
Ming-Qing Li1 Obstetrics and Gynecology Hospital, Fudan University, Shanghai, People's Republic of China.
Xiang-Hong Xu2 Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China.
Cong-Jian Xu1 Obstetrics and Gynecology Hospital, Fudan University, Shanghai, People's Republic of China.
Obstetrics and Gynecology Hospital of Fudan University · CNShanghai First Maternity and Infant Hospital · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDecidual γδ T cells are known to regulate the function of trophoblasts at the maternal-fetal interface; however, little is known about the molecular mechanisms of cross talk between trophoblast cells and decidual γδ T cells.

methodsExpression of chemokine C-X-C motif ligand 6 (CXCL16) and its receptor CXCR6 was evaluated in first-trimester human villus and decidual tissues by immunohistochemistry. γδ T cells were isolated from first-trimester human deciduae and cocultured with JEG3 trophoblast cells. Cell proliferation and apoptosis-related molecules, together with cytotoxicity factor and cytokine production, were measured by flow cytometry analysis.

resultsExpression of CXCL16 and CXCR6 was reduced at the maternal-fetal interface in patients who experienced unexplained recurrent spontaneous abortion as compared to healthy pregnancy women. With the administration of pregnancy-related hormones or coculture with JEG3 cells, CXCR6 expression was upregulated on decidual γδ T cells. CXCL16 derived from JEG3 cells caused a decrease in granzyme B production of decidual γδ T cells. In addition, decidual γδ T cells educated by JEG3-derived CXCL16 upregulated the expression of Bcl-xL in JEG3 cells.

conclusionThis study suggested that the CXCL16/CXCR6 axis may contribute to maintaining normal pregnancy by reducing the secretion of cytotoxic factor granzyme B of decidual γδ T cells and promoting the expression of antiapoptotic marker Bcl-xL of trophoblasts.

Indexed as

bcl-X ProteinCells, CulturedCell SurvivalChemokine CXCL16Chorionic VilliDeciduaFemaleGranzymesHumansPregnancyPregnancy Trimester, FirstReceptors, CXCR6TrophoblastsBCL2L1 protein, humanbcl-X ProteinChemokine CXCL16CXCL16 protein, humanCXCR6 protein, humanGranzymesReceptors, CXCR6CXCL16CXCR6decidual γδ T cellstrophoblastsunexplained recurrent spontaneous abortion

Identifiers

PMID29909746
PMCPMC6421627
OpenAlexW2808982585

What OpenQuestion holds

Textmetadata
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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.