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The Role of Complement and CD4 T Cells in Preeclampsia and Offspring Neurodevelopment
Jean F Regal1, Courtney A O'Kane1, Sabrina M Scroggins1
1Department of Biomedical Sciences, University of Minnesota Medical School, Duluth Campus, 1035 University Dr, Duluth, MN 55812 USA.
Insights
Preeclampsia, a pregnancy disorder, involves immune system imbalances affecting maternal health and fetal brain development. Understanding complement and T helper cell interactions is key to addressing these neurodevelopmental risks.
Area of Science:
- Immunology
- Obstetrics
- Neuroscience
Background:
- Preeclampsia is a complex hypertensive disorder of pregnancy.
- Immune dysregulation, including complement and T helper cell imbalances, contributes to preeclampsia pathology.
- Prenatal exposure to preeclampsia is linked to increased neurodevelopmental disorders in children.
Purpose of the Study:
- To explore the link between immune dysregulation in preeclampsia and altered fetal brain development.
- To investigate the role of complement and T helper cell interactions in preeclampsia-associated neurodevelopmental outcomes.
Main Methods:
- Review of clinical and experimental data on preeclampsia, complement pathways, and T helper cell responses.
- Analysis of immune signaling at the maternal-fetal interface.
- Examination of potential mechanisms linking maternal inflammation to fetal brain development.
Main Results:
- Preeclampsia is associated with dysregulated complement activity and skewed T helper cell responses (↑TH1/TH17, ↓Treg).
- These immune alterations may lead to increased fetal exposure to inflammatory signals.
- Converging evidence suggests a connection between maternal immune dysregulation and altered fetal brain development.
Conclusions:
- Immune dysregulation at the maternal-fetal interface, driven by complement and T helper cell interactions, is implicated in preeclampsia.
- This immune imbalance may mediate altered fetal brain development and subsequent neurobehavioral effects.
- Further research is needed to define the precise mechanisms, timing, and tissue compartments of these interactions.
Abstract:
Preeclampsia is a multifactorial hypertensive disorder of pregnancy. Dysregulated innate complement activity and skewing of adaptive CD4+ T helper (TH) responses (↑TH1/TH17, ↓Treg) contribute to maternal hypertension, endothelial dysfunction, and proteinuria. Children exposed in utero to preeclampsia have higher rates of neurodevelopmental disorders. Because complement and TH pathways also shape normal neurodevelopment, converging clinical and experimental data link preeclampsia to immune dysregulation at the maternal-fetal interface, increased fetal exposure to inflammatory signals, and altered fetal brain development with downstream neurobehavioral effects. Interactions between complement (e.g., C3a/C5a) and TH cells is a plausible driver of these effects, but the precise mechanisms, timing, and tissue compartments remain to be defined.
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