Evidence map›Paper›PMID 29588487›Full record

ArticleCellular & molecular immunology2018

Trophoblast-derived CXCL16 induces M2 macrophage polarization that in turn inactivates NK cells at the maternal-fetal interface.

Xiao-Qiu Wang, Wen-Jie Zhou, Xin-Xin Hou, Qiang Fu, Da-Jin Li

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Metabolic Reprogramming Driven by Trophoblasts and Decidual XCR1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  19. Review
  20. Infection and immunity · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Xiao-Qiu WangLaboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital and Institute of Obstetrics and Gynecology, IRD, Fudan University, Shanghai Medical College, Shanghai, China.
Wen-Jie ZhouLaboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital and Institute of Obstetrics and Gynecology, IRD, Fudan University, Shanghai Medical College, Shanghai, China.
Xin-Xin HouLaboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital and Institute of Obstetrics and Gynecology, IRD, Fudan University, Shanghai Medical College, Shanghai, China.
Qiang FuCollege of Basic Medicine, Binzhou Medical University, Yantai, Shandong, China.
Da-Jin LiLaboratory for Reproductive Immunology, Key Laboratory of Reproduction Regulation of NPFPC, SIPPR, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital and Institute of Obstetrics and Gynecology, IRD, Fudan University, Shanghai Medical College, Shanghai, China. djli@shmu.edu.cn.
Shanghai Institute of Planned Parenthood Research · CNBinzhou University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decidual macrophages (dMΦ) are distinct from the conventional macrophages present in other tissues and express M2 macrophage markers, but the molecular mechanisms of formation and the roles of M2 MΦ during pregnancy have not been completely elucidated. The crosstalk between decidual natural killer cells (dNK) and dMΦ plays an important role in the maintenance of maternal-fetal immune tolerance. Here, CXCL16 derived from first-trimester trophoblast cells induces the polarization of human M2 macrophages. The M2 MΦ polarized by CXCL16 exhibit decreased interleukin-15 production, which facilitates the inactivation of NK cells. The cytotoxicity of NK cells is attenuated by the CXCL16-polarized M2 MΦ. The data shown in the present study provide evidence to support the hypothesis that CXCL16 secreted by trophoblast cells is a key molecule involved in decidual M2 MΦ polarization, which in turn regulates the killing ability of NK cells, thereby contributing to the homeostatic and immune-tolerant milieu required for successful fetal development.

Indexed as

Cell CommunicationCell DifferentiationCells, CulturedChemokine CXCL16CytokinesCytotoxicity, ImmunologicDeciduaFemaleHomeostasisHumansImmune ToleranceInterleukin-15Killer Cells, NaturalMacrophagesMaternal-Fetal ExchangePregnancyChemokine CXCL16CXCL16 protein, humanCytokinesInterleukin-15CXCL16macrophage polarizationmaternal–fetal interfaceNK cellstrophoblasts

Identifiers

PMID29588487
PMCPMC6269500
OpenAlexW2794998265

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.