Transcriptome analysis suggests a central role for complement and C5aR1 in neutrophil activation in APS

Antiphospholipid syndrome (APS) is characterized by thrombosis and/or recurrent pregnancy loss in the presence of persistently positive antiphospholipid antibodies (aPL). APS, particularly the most severe variant, catastrophic APS (CAPS) is associated with complement activation and a high incidence of complement regulatory gene mutations [1]; moreover, complement inhibition has been effective in preventing recurrent thrombosis in some patients with APS [2]. The pathogenesis of thrombosis in APS is not well understood, and likely multifactorial [3].