Abstract: Objective：To investigate the roles of Toll-like receptor 4 (TLR4) in the expressions of adhesion molecules and tissue factor (TF) in mouse artery induced by anti-β2-glycoprotein Ⅰ (β2GPⅠ) antibody. Methods：TLR4-intact C3H/HeN mice and TLR4-defective C3H/HeJ mice were pretreated for 72 h by intraperitoneal injection with anti-β2GPⅠ antibody. Then, the expressions of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin proteins in arterial endothelium were detected by an immunohistochemistry method. The levels of ICAM-1, VCAM-1 and E-selectin mRNA and proteins in artery homogenates were detected by real-time quantitative PCR (qRT-PCR) and western blot, respectively. The TF activity and mRNA level in artery homogenates were determined by a commercial TF activity detection kit and qRT-PCR, respectively. Results：The expressions of ICAM-1, VCAM-1 and E-selectin in arterial endothelium of C3H/HeN mice increased significantly after induction with anti-β2GPⅠ antibody. Compared with normal saline control group, the expression levels of ICAM-1, VCAM-1 and E-selectin mRNA and proteins in artery homogenates of C3H/HeN and C3H/HeJ mice were significantly up-regulated by anti-β2GPⅠ antibody (P<0.05). However, the expression levels of ICAM-1, VCAM-1 and E-selectin mRNA and proteins in C3H/HeJ mice were significantly lower than those in C3H/HeN mice (P<0.05). Similarly, TF mRNA and activity in artery homogenates of C3H/HeN mice induced with anti-β2GPⅠ antibody were significantly lower than that in C3H/HeJ mice (P<0.05). Conclusion：TLR4 contributes to the expressions of ICAM-1, VCAM-1, E-selectin and TF in mouse artery induced by anti-β2GPⅠ antibody. However, its molecular mechanism and correlation with the thrombosis pathogenesis of antiphospholipid syndrome (APS) remain to be further studied.