# Immune Cells in Preeclampsia

## TL;DR

Preeclampsia involves immune cell activity that causes inflammation and tissue damage, potentially offering new treatment targets.

## Contribution

The paper highlights the specific roles of T cells, B cells, Natural Killer cells, and macrophages in preeclampsia's immune response.

## Key findings

- T helper cells and B cells contribute to chronic inflammation and autoantibody production in preeclampsia.
- Natural Killer cells shift to a cytotoxic state, promoting tissue damage in the disease.
- Macrophages adopt a proinflammatory state, worsening inflammation and organ dysfunction.

## 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.