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Published on: January 26, 2024
Immune Cells in Preeclampsia
Nathan Campbell1, Marcus Robbins1, Hellen Nembaware1
1Department of Pharmacology & Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Insights
Preeclampsia involves pregnancy-induced hypertension linked to chronic inflammation. Immune cells like T cells, B cells, and macrophages contribute to placental and organ damage, suggesting immunotherapy as a potential treatment.
Area of Science:
- Immunology
- Obstetrics
- Pathophysiology
Background:
- Preeclampsia (PE) is characterized by new-onset hypertension during pregnancy.
- PE is associated with chronic inflammation in the placenta and systemically.
- Placental ischemia in PE triggers anti-angiogenic factors and inflammatory mediators, leading to organ damage.
Purpose of the Study:
- To investigate the role of the immune system in preeclampsia pathophysiology.
- To explore immune cell involvement in placental and systemic inflammation during PE.
- To identify potential therapeutic targets within the immune system for improved maternal and fetal outcomes.
Main Methods:
- Review of existing literature on immune cell function in preeclampsia.
- Analysis of inflammatory mediators and cellular pathways implicated in PE.
- Examination of the contribution of T cells, B cells, Natural Killer cells, and macrophages.
Main Results:
- T helper cells promote chronic inflammation and activate B cells to produce autoantibodies.
- Natural Killer cells shift towards a cytotoxic phenotype, contributing to tissue damage.
- Macrophages polarize to proinflammatory subtypes, exacerbating inflammation and tissue damage.
Conclusions:
- The immune system plays a critical role in preeclampsia development and progression.
- Immune dysregulation contributes to placental, renal, and vascular damage in PE.
- Targeting immune pathways offers a promising strategy for therapeutic interventions in preeclampsia.
Abstract:
Preeclampsia (PE), new-onset hypertension during pregnancy, is associated with chronic inflammation both in the placenta and systemically. PE is characterized by placental ischemia, which then results in the production and release of anti-angiogenic factors and inflammatory mediators. Inflammation in PE leads to placental, renal, and vascular damage, which contribute to the phenotype of hypertension and organ dysfunction during pregnancy. T cells, B cells, Natural Killer cells, and macrophages have all been shown to play a role in the inflammation present in the disease. T helper cells contribute to the chronic inflammation in PE. They also activate B cells, which produce agonistic autoantibodies against the angiotensin II type 1 receptor. Natural Killer cells are activated in PE and shift away from decidual Natural killer cells, which produce angiogenic factors, and toward cytotoxic Natural Killer cells, which contribute to tissue damage. Macrophages are polarized towards proinflammatory subtypes and contribute to tissue damage and inflammatory signaling in PE patients. As the immune system plays a role in the pathophysiology of the disease, it may be a potential target for therapeutic intervention to improve maternal and fetal outcomes during and following a PE pregnancy.
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