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Abstract P216: Inhibition Of T Cell Activation In Response To Placental Ischemia During Pregnancy Improves Hypertension And Activation Of Natural Killer Cells


 Preeclampsia (PE), new onset hypertension during pregnancy, is the leading cause of death and morbidity world-wide for the mother and fetus during pregnancy. The Reduced Uterine Perfusion Pressure Rat Model of PE (RUPP) exhibits many characteristics of PE including hypertension, suppressed regulatory T cells (T
 RegS
 ) associated with increased CD4+ T cells and B cells secreting agonistic autoantibodies to the AngII receptor (AT1-AA). We have previously shown that blockade of T-helper cells improves blood pressure and lowers AT1-AA secretion. A potential mechanism for the decreased blood pressure is decreased cytolytic natural killer (cNK) cells. Abatacept (Aba) is a fusion molecule designed to inhibit T cell co-stimulation in response to antigens and is used to treat autoimmune diseases. We hypothesize that treatment with Aba will prevent the activation of T-helper cells and therefore lower AT1-AA as a mechanism leading to less cNK cells in response to placental ischemia in RUPP rats. Aba was given on day 13 via the jugular vein. On day 19, blood and tissues were collected, blood pressure (MAP), pup weight, and NK cells were measured by flow cytometry in the blood and placenta. A one-way ANOVA was used for statistical analysis. On GD19, MAP significantly increased in RUPP 119±2 mmHg (n=7, p<0.05) compared to NP controls 102±2 mmHg (n=7) and was normalized with Aba (100±2 mmHg (n=10, p<0.05). Compared to the NP controls (2.2±0.06, n=7), pup weight significantly decreased in RUPP (2±0.08, n=7, p<0.05) but was 2± 0.07, with Aba (n=10). Circulating and placental total NK cells were 32±5, 44±13, % gate in NP rats (n=7), 59±4, 60±16 % gate in RUPP rats (n=7, p<0.05; n=4), which significantly decreased to 40±6, 28±8 % gate with Aba (n=10, p<0.05; n=11). Our findings indicate that prevention of T cell activation lowers total NK cell number and blood pressure in response to placental ischemia of pregnancy.
