“…The affected endothelium is a focus of platelet activation, which leads to the formation of blood clots and reactive oxygen species [4][5][6]. Adhesion molecules, together with chemokines, are activated by the damaged endothelium to attract leukocytes, which ensures the development of both innate and adaptive immune responses, including loss of tolerance to autoantigens, for instance, topoisomerase I [7,8]. Antibodies against topoisomerase I form immune complexes, are absorbed through Fc-receptors and activate endosomal Toll-like receptors in immune cells, which leads to the production of type I interferon.…”