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Published on: May 24, 2024
Recent Developments in Macrophages Imbalance and Recurrent Spontaneous Abortion
Yi Xiao1, Fan-Yu Zeng2, Jin-Song Liu1
1Department of Obstetrics and Gynecology, General Hospital of Northern Theater Command, Shenyang 110000, Liaoning Province, China, syjqzyy.com.
Journal of Immunology Research
|July 24, 2026
Summary
Immune dysregulation involving macrophages contributes to recurrent spontaneous abortion (RSA). An imbalance favoring pro-inflammatory M1 macrophages over M2 macrophages disrupts pregnancy, leading to fetal loss.
Area of Science:
- Reproductive Medicine
- Immunology
- Developmental Biology
Background:
- Recurrent spontaneous abortion (RSA) is a significant reproductive health challenge.
- Immune dysregulation, particularly macrophage imbalance, is implicated in RSA pathogenesis.
- Macrophages in the decidua play crucial roles in pregnancy by influencing trophoblast invasion and placental development.
Purpose of the Study:
- To review the mechanisms linking immune dysregulation and recurrent spontaneous abortion (RSA).
- To elucidate the role of macrophage polarization in RSA.
- To highlight potential research directions for improving clinical outcomes in RSA.
Main Methods:
- Literature review integrating human studies and animal models.
- Analysis of molecular and cellular mechanisms underlying macrophage polarization.
- Examination of factors influencing the M1/M2 macrophage balance.
Main Results:
- Aberrations in transcription factors, signaling pathways, cytokines, epigenetics, and metabolism drive macrophage polarization towards the M1 phenotype.
- An elevated M1/M2 macrophage ratio promotes pro-inflammatory cytokine secretion.
- This immune imbalance impairs trophoblast invasion and placental angiogenesis, contributing to spontaneous abortion.
Conclusions:
- Immune dysregulation, specifically M1 macrophage polarization, is a key mechanism underlying recurrent spontaneous abortion (RSA).
- Understanding these immune pathways offers targets for therapeutic interventions.
- Further research is needed to translate these findings into improved clinical management of RSA.

