SAT0287 TH1, TH2 and TH17 lymphoid subpopulations in primary antiphospholipid syndrome

Background Primary antiphospholipid antibody syndrome (PAPS) is characterized by thrombosis at different levels and maternal fetal complications in the presence of antiphospholipid antibodies (aPL). Lymphoid subpopulations and cellular immune responses have not been fully studied. Objectives To analyze the lymphoid subpopulations, Th1, Th2 and Th17 immune response in patients with PAPS and long term evolution. Methods Patients with PAPS,>18 years of age, of both sexes and a group of healthy blood donors matched for age and sex were included. All patients were receiving oral anticoagulants (Coumadin type). No patient had a recent episode of thrombosis or other manifestation of APS at the time of the study. Peripheral blood was obtained and lymphoid subpopulations were determined by flow cytometry in order to identified with specific immunological markers for Treg cells: CD4+/CD25+/FoxP3+ and CD8+/CD25+/FoxP3+. The dendritic cells analyzed were: Type 1: Lin1- HLA-DR+/CD11c+; Type 2: Lin-HLA-DR+/CD123+; B lymphocytes with antiCD19-APC; Monocytes with anti-CD14-PE; NK: CD3-/CD16+56+ and NKT: CD3+/CD16+56+ lymphocytes. Th1 cells were identified by IFN-g+ positivity; Th2: positivity for IL-4+; Th17: positivity for IL-17+. Parametric statistics and Mann-Whitney U-test were used. Results A total of 39 patients with PAPS were included, age: 51.9±12.8, evolution time: 12.8±8.9 years and 35 healthy controls. In patients with PAPS there was a decrease in the total CD8 count (p Conclusions This study shows profound alterations in innate and adaptive immunity in patients with long-term PAPS, characterized by a decrease in certain lymphocyte subpopulations, with consequent functional alteration. These abnormalities can become new therapeutic targets in order to restore immune imbalance. Our findings may explain in part, the development of thrombosis and other complications, despite treatment with oral anticoagulants in PAPS patients with long term disease evolution. References Dal Ben ER, do Prado CH, Baptista TS, Bauer ME, Staub HL. Decreased levels of circulating CD4+CD25+Foxp3+regulatory T cells in patients with primary antiphospholipid syndrome. J Clin Immunol 2013; 33: 876–879. Xiao J, Zhu F, Liu X, Xiong J.Th1/Th2/Th17/Treg expression in cultured PBMCs with antiphospholipid antibodies.Mol Med Rep. 2012;6(5):1035–9. Jakiela B, Iwaniec T, Plutecka H, Celinska-Lowenhoff M, Dziedzina S, Musial J. Signs of impaired immunoregulation and enhanced effector T-cell responses in the primary antiphospholipid syndrome. Lupus. 2016; 25(4):389–98. Disclosure of Interest None declared