Figure 4

Mechanisms of peripheral blood cells in the pathogenesis of UC. (A) Peripheral blood cells enter from blood into the intestine and mediate the inflammatory response to damage the intestinal barrier. (B) The activated platelets participated in dysfunction of intrinsic and extrinsic blood coagulation. Solid black arrows represented “conversion to”, dashed black arrows represented “release”, red arrows represented “promotion”, green arrows represented “inhibition”, and blue arrows represented “increase and decrease of substances”. APC activated protein C, CD cluster of differentiation, CRP C reactive protein, ENA extractable nuclear antigen, EPCR endothelial protein C receptor, EPCR endothelial protein C receptor, EPO erythropoietin, Fg fibrinogen, GM-CSF granulocyte–macrophage colony-stimulating factor, GP glycoprotein, HETE hydroxy eicosatetraenoic acid, HLA human leukocyte antigen, ICAM intercellular adhesion molecule, IL interleukin, L ligand, MAC membrane attack complex, MCP monocyte chemotactic protein, MPO myeloperoxidase, PAF platelet-activating factor, PC protein C, PDGF platelet-derived growth factor, PF platelet factor, PLAs platelet-leukocyte aggregates, P-LEV platelet-derived large extracellular vesicle, PSGL P-selectin glycoprotein ligand, RANTES regulated upon activation, normal T cell expressed and presumably secreted, ROS reactive oxygen species, TCR T cell receptor, TF tissue factor, TFPI tissue factor pathway inhibitor, Th T helper cell, TL1A tumor necrosis factor-like ligand 1, TLR toll-like receptor, TM thrombomodulin, TNF tumor necrosis factor, TPO thrombopoietin, TXA thromboxane, UC ulcerative colitis, VWF von Willebrand factor.