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Updated: Sep 16, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

Published on: January 26, 2024

Systemic and Local Immunological Markers in Preeclampsia.

Almagul Kurmanova¹, Altynay Nurmakova^2,3, Damilya Salimbayeva^2,3

¹Department of Obstetrics and Gynecology, Al-Farabi Kazakh National University, 71 Al-Farabi Ave., 050040 Almaty, Kazakhstan.

Diagnostics (Basel, Switzerland)

|July 12, 2025

Summary

Preeclampsia involves immune system changes in both maternal blood and placenta. Dysregulation of immune cells like T, B, and NK cells contributes to inflammation and oxidative stress, impacting pregnancy outcomes.

Keywords:

cytokines immune system maternal medicine placenta pre-eclampsia

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Area of Science:

Immunology
Obstetrics
Perinatology

Background:

Preeclampsia (PE) is a leading cause of maternal and neonatal mortality.
The maternal immune system balances pathogen defense and tolerance to the semi-allogenic fetus.
Immune dysregulation is implicated in PE pathogenesis.

Purpose of the Study:

To compare immunological markers in maternal blood and placenta between preeclampsia and normal pregnancies.
To investigate immune cell subpopulations and cytokine profiles.

Main Methods:

Comparative study of 35 pregnant women (7 PE, 28 controls).
Flow cytometry analysis of peripheral blood and placental tissue.
Assessment of lymphocyte subpopulations and intracellular cytokine production.

Main Results:

PE blood showed decreased CD14+ monocytes, increased NK cells (CD16+, CD56+), and activation markers (HLA-DR+, CD95+).
Elevated IL-10, TNF, Perforin, GM-CSF, and IGF were found in PE blood.
PE placenta exhibited decreased regulatory cells (CD4+, CD8+, CD14+, CD56+, CD59+), activation markers (CD95+), IL-10, VEGFR, and IGF.

Conclusions:

The maternal-fetal immune profile is critical for fetal development.
Dysregulation of T, B, and NK cells contributes to inflammation, oxidative stress, and preeclampsia development.