The role of complement and CD4 T cells in preeclampsia and offspring neurodevelopment
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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