Antiphospholipid syndrome (APS) is an autoimmune disease characterized by antiphospholipid antibodies, thrombosis and pregnancy morbidity. APS occurs in about 20% of patients with systemic lupus erythematosus (SLE) but may also present as a stand-alone disorder reffered to as "primary" APS (PAPS).
In this thesis we studied the immune system in patients with PAPS as compared to patients with SLE. Amongs others we studied the role of the interferon signature, release of neutrophil extracellular traps (NETs) and B-cell activating factor (BAFF) in PAPS. Furthermore we provided an in depth analysis of circulating dendritic cells by means of RNA sequencing and microRNA profiling and identified several dysregulated pathways in these cells which may open up new avenues for therapeutic intervention.