Objective:

To investigate the role of FOLR2+ macrophages in the decidua and their impact on immune activation, decidualization, and angiogenesis in recurrent spontaneous abortion (RSA).

Approach:

Key Findings:

• FOLR2+ macrophages in the decidua exhibit an M2-like immunoregulatory phenotype.
• In RSA decidua, FOLR2 expression and the proportion of FOLR2+ macrophages are markedly reduced.
• Reduction in FOLR2+ macrophages correlates with increased inflammatory signaling and impaired angiogenic interactions.
• FOLR2 overexpression enhances immunoregulatory and pro-angiogenic properties.
• FOLR2 silencing promotes inflammatory responses and impairs angiogenesis.

Interpretation:

The loss of FOLR2+ macrophages in RSA may contribute to immune dysregulation and defective decidualization.

Limitations:

• The study primarily focuses on human decidua and may not fully represent other contexts of spontaneous abortion.
• Further research is needed to explore the mechanisms underlying the observed changes in macrophage populations.

Conclusion:

FOLR2+ macrophages are crucial for maintaining immune tolerance and supporting decidualization at the maternal–fetal interface.

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