Abnormal Expression of the LAG-3/FGL-1 Signaling Pathway in Patients with Early-Onset Preeclampsia
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Updated: Aug 26, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Yue Liang1, Yining Liu1, Shan Wang2
1Department of Obstetrics and Gynecology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China (mainland).
Abstract:
BACKGROUND Preeclampsia (PE) is a serious pregnancy disorder associated with immune tolerance imbalance. The etiology of preeclampsia has not been fully elucidated. The aim of this study was to clarify the possible role of the lymphocyte activation gene 3 (LAG-3)/fibrinogen-like protein 1 (FGL-1) signaling pathway in the immune imbalance of early-onset PE. MATERIAL AND METHODS We enrolled 34 women with early-onset PE and 34 age-matched normal pregnancies (NPs). Flow cytometry was performed to determine the expression of LAG-3 on peripheral T cell subsets (CD3+, CD4+, and CD8+ T cells). We measured LAG-3 expression on decidual T cells to determine whether there was a difference in the expression of LAG-3 between decidual and peripheral T cells. Maternal plasma levels of FGL-1 were measured by ELISA. RESULTS There was no significant difference in LAG-3 expression on peripheral CD3+ T cells between NP and early-onset PE. Compared to NP, the significant decrease expression of LAG-3 by peripheral CD4+ and CD8+T cells was found in early-onset PE. The LAG-3 expression was higher on decidual T cells than peripheral counterparts in all pregnancies. The plasma level of FGL-1 was significantly elevated in early-onset PE compared with NP. CONCLUSIONS Abnormal expression of LAG-3/FGL-1 signaling pathway may be associated with immune activation of effector T cells and impaired immune tolerance in early-onset PE.
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