ReviewFrontiers in bioengineering and biotechnology2021
Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia.
Review in Frontiers in bioengineering and biotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Gut microbiome and pregnancy complications: emerging evidence and mechanistic insights.Gut microbes · 2026Review
- CCR5 blockade inhibits menstrual-driven proinflammatory T cell infiltration into the cervicovaginal mucosa of women.Science advances · 2026Article
- Article
- Regulation of PI3K/Akt in preeclampsia: an examination of its pathological role and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Single-cell analysis of uterine artery endothelial cells reveals cytokine-induced emergence of specific immunomodulatory subtypes: implications for preeclampsia.Journal of molecular endocrinology · 2025Article
- Uric Acid and Preeclampsia: Pathophysiological Interactions and the Emerging Role of Inflammasome Activation.Antioxidants (Basel, Switzerland) · 2025Review
- Integrated multi-omics analysis reveals immunovascular mechanisms of the placenta-maternal brain axis and lifespan neurobehavior changes in a mouse model of preeclampsia.Neuroscience · 2025Article
- Preeclamptic Placental CD19+ B Cells Are Causal to Hypertension During Pregnancy.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Evaluating oxidative stress targeting treatments inFrontiers in cell and developmental biology · 2025Article
- Early prediction of preeclampsia using the first trimester vaginal microbiome.bioRxiv : the preprint server for biology · 2024Article
- Anti-angiogenic mechanisms and serotonergic dysfunction in the Rgs2 knockout model for the study of psycho-obstetric risk.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Low indoleamine 2, 3 dioxygenase (IDO) activity is associated with psycho-obstetric risk.Pregnancy hypertension · 2024Article
- Development and validation of preeclampsia predictive models using key genes from bioinformatics and machine learning approaches.Frontiers in immunology · 2024Article
- A role for adverse childhood experiences and depression in preeclampsia.Journal of clinical and translational science · 2024Article
- The Role of ncRNAs in the Immune Dysregulation of Preeclampsia.International journal of molecular sciences · 2023Review
- Maternal and fetal mitochondrial gene dysregulation in hypertensive disorders of pregnancy.Physiological genomics · 2023Article
- Increased fetal microchimerism in immune and stem cell subsets in preeclampsia.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Setting a stage: Inflammation during preeclampsia and postpartum.Frontiers in physiology · 2023Review
- Update on Immune Mechanisms in Hypertension.American journal of hypertension · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Preeclampsia (PreE) is a placental disorder characterized by hypertension (HTN), proteinuria, and oxidative stress. Individuals with PreE and their children are at an increased risk of serious short- and long-term complications, such as cardiovascular disease, end-organ failure, HTN, neurodevelopmental disorders, and more. Currently, delivery is the only cure for PreE, which remains a leading cause of morbidity and mortality among pregnant individuals and neonates. There is evidence that an imbalance favoring a pro-inflammatory CD4+ T cell milieu is associated with the inadequate spiral artery remodeling and subsequent oxidative stress that prime PreE's clinical symptoms. Immunomodulatory therapies targeting CD4+ T cell mechanisms have been investigated for other immune-mediated inflammatory diseases, and the application of these prevention tactics to PreE is promising, as we review here. These immunomodulatory therapies may, among other things, decrease tumor necrosis factor alpha (TNF-α), cytolytic natural killer cells, reduce pro-inflammatory cytokine production [e.g. interleukin (IL)-17 and IL-6], stimulate regulatory T cells (Tregs), inhibit type 1 and 17 T helper cells, prevent inappropriate dendritic cell maturation, and induce anti-inflammatory cytokine action [e.g. IL-10, Interferon gamma (IFN-γ)]. We review therapies including neutralizing monoclonal antibodies against TNF-α, IL-17, IL-6, and CD28; statins; 17-hydroxyprogesterone caproate, a synthetic hormone; adoptive exogenous Treg therapy; and endothelin-1 pathway inhibitors. Rebalancing the maternal inflammatory milieu may allow for proper spiral artery invasion, placentation, and maternal tolerance of foreign fetal/paternal antigens, thereby combatting early PreE pathogenesis.
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Registered trials
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