Placental CD4+ T cells from preeclamptic patients cause autoantibodies to the angiotensin II type I receptor and hypertension in a pregnant rat model of preeclampsia

Aim: Preeclampsia (PE) is a hypertensive disorder of pregnancy associated with activated CD4+ T cells and autoantibodies to angiotensin II type 1 receptor (AT1-AA). We have previously shown that isolated from women PE cause hypertension, increased tumor necrosis factor alpha (TNF-α), endothelin-1, soluble fms-like tyrosine kinase-1 (sFlt-1) when injected into pregnant nude-athymic rats compared normal (NP) women. However, the role AT1-AA as mechanism hypertension not known. Our goal was determine if stimulate in rats. Methods: were human NP placentasand on gestational day (GD) 12. In order examine B cell secretion AT1-AA, subset receiving treated rituximab GD 14 or anti-CD40 ligand (anti-CD40L) On 19, mean arterial pressure (MAP) tissues obtained. Results: MAP [114 ± mmHg (n = 9)] [19.8 0.9 beats per minute (bpm, n 4)] nude + [98 2 7, P < 0.05) 1.3 bpm 5, 0.05)]. Rituximab (103 mmHg, 3, anti-CD40L (102 lowered cells. Circulating proliferation-inducing (APRIL) placental angiotensin-converting enzyme (ACE-2) activity response Conclusions: These results show play an important pathophysiology PE, by activating secreting during pregnancy.