“…The release of vasoconstrictor agents exceeds the release of vasodilator agents leading to vascular instability. 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].…”