Evidence map›Paper›PMID 41280905›Full record

ArticleFrontiers in immunology2025

Reciprocal activation between M1 macrophages and trophoblasts through CXCL9/STAT1/ZEB1/CCL2 axis promotes recurrent spontaneous abortion.

Sisi Yan, Xiang Wang, Qiuji Wu, Jinli Ding, Hui Qiu

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

1 citing paper in PubMed.

  1. Review
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.

Sisi Yan *Department of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Cancer Clinical Study Center, Zhongnan Hospital of Wuhan University, Wuhan, China.
Xiang Wang *Department of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Cancer Clinical Study Center, Zhongnan Hospital of Wuhan University, Wuhan, China.
Qiuji WuDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Cancer Clinical Study Center, Zhongnan Hospital of Wuhan University, Wuhan, China.
Jinli DingReproductive Medical Center, Renmin Hospital of Wuhan University and Hubei Clinic Research center for Assisted Reproductive Technology and Embryonic Development, Wuhan, China.
Hui QiuDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Cancer Clinical Study Center, Zhongnan Hospital of Wuhan University, Wuhan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The crosstalk between macrophages and trophoblasts plays a crucial role in the development and progression of recurrent spontaneous abortion (RSA). Although M1 macrophages (M1-Mφ) are known to accumulate in RSA decidual tissues, their direct functional impact on trophoblasts remains poorly characterized. Methods: We established an M1-Mφ-trophoblast coculture system to investigate this interaction. CXCL9 expression was quantified in clinical samples and cell lines using qPCR, ELISA, and immunofluorescence. The migration and invasion capacities of trophoblasts were evaluated through wound healing and Transwell assays. A series of rescue experiments were conducted to uncover the underlying mechanism. Finally, an Results: Our results revealed that M1-Mφ inhibited the migration and invasion of trophoblasts by releasing CXCL9. The expression of CXCL9 in decidual tissues was significantly increased in RSA samples compared to healthy controls. Mechanistically, CXCL9 activated the CXCR3-dependent JAK/STAT1 signaling pathway. Activated STAT1 induced transcriptional upregulation of ZEB1 via IRF1, which in turn promoted the release of CCL2 to enhance macrophage recruitment. Conclusion: Our work identifies a novel mechanism by which M1-Mφ regulate trophoblast migration and invasion through the CXCL9/STAT1/IRF1/ZEB1 axis, which in turn leads to the release of CCL2 that promotes macrophage infiltration in RSA, highlighting a new form of crosstalk between macrophages and trophoblasts.

Indexed as

Abortion, HabitualChemokine CCL2Chemokine CXCL9Macrophage ActivationMacrophagesSTAT1 Transcription FactorTrophoblastsAdultAnimalsCell MovementFemaleHumansMicePregnancySignal TransductionCCL2 protein, humanChemokine CCL2Chemokine CXCL9CXCL9 protein, humanSTAT1 protein, humanSTAT1 Transcription FactorCXCL9EMTM1-Mφmigration and invasionrecurrent spontaneous abortiontrophoblasts

Identifiers

PMID41280905
PMCPMC12634548

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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.