1003 Suppressor of cytokine signaling-1: a potential mechanistic target the immune system imbalance in preeclampsia development

Abstract

Although the etiology of preeclampsia (PEC) is not completely understood, the importance of abnormal placentation in disease development is well established. This abnormal placentation is thought to be due to an immune system imbalance, characterized by an increase in proinflammatory CD4+T cells, and a decrease in regulatory T cells (Tregs). To date, the mechanism by which this imbalance develops is unknown. Notably, Suppressor of Cytokine Signaling-1 (SOCS1) is an important regulator of proinflammatory CD4+ T cells. It also plays a major role in maintaining the stability of Tregs. Moreover, SOCS1 deficiency leads to autoimmune disease development, as SOCS1 deficient mice develop lupus, and lupus patients have reduced SOCS1 expression. Given that disease development in PEC results from an imbalance toward a proinflammatory state, the objective of this study is to determine whether there are differences in SOCS1 expression between PEC patients and controls. SOCS1 mRNA expression was measured from maternal whole blood drawn during delivery admission from patients with PEC, per ACOG guidelines, and controls. All participants were women with singleton pregnancies, >37 weeks. Controls were matched for gestational age, race, and ethnicity. Exclusion criteria: patients with autoimmune disease, chronic viral infection, and/or on immunosuppressants. RNA was isolated from whole blood and analyzed using NanoDrop technology. Following cDNA synthesis, SOCS1 mRNA expression was determined by qPCR. n=5 for each group. Statistical analysis: two-tailed T test. SOCS1 expression is significantly decreased in PEC patients in comparison to controls. SOCS1 expression was decreased in this small cohort of PEC patients. Given that SOCS1 prevents uncontrolled proinflammatory cytokine expression, these preliminary results suggest that decreased SOCS1 expression in a larger cohort of PEC patients could serve as a mechanistic target for the study of the immune system imbalance in PEC development.