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. Author manuscript; available in PMC: 2021 Oct 6.
Published in final edited form as: Circulation. 2020 Oct 5;142(14):1389–1398. doi: 10.1161/CIRCULATIONAHA.120.048186

Figure 1. Mechanisms participating in porcine endothelial injury by human blood.

Figure 1.

Preformed human anti-pig antibodies bind to porcine endothelium, triggering complement binding and Fc-receptor–mediated ligation of platelets and leukocytes and upregulation of adhesion molecules on both adherent formed blood elements and inflamed endothelium. Complement cascade activation (orange symbols), nonphysiological adhesion of human platelets to porcine endothelium, and absence of nonself signals (illustrated for natural killer cells) contribute to a prothrombotic, proinflammatory milieu that leads to loss of vascular barrier function and organ failure. GP indicates glycoprotein; ICAM, intercellular adhesion molecule; IL-6, interleukin-6; PMN, polymorphonuclear; PSGL-1, P-selectin glycoprotein ligand 1; TNF, tumor necrosis factor; and vWF, von Willebrand factor.