“…The precise mechanisms underlying the pathogenesis of APS remain unclear; however, a multifactorial process similar to other autoimmune diseases has been posited involving a complex interplay between genetic predisposition, antigenic stimuli, and the presence of specific autoantibodies. APS is thought to involve the activation of several cell types, such as endothelial cells, monocytes, platelets, and trophoblast cells, the activation of the coagulation and complement systems, and the inhibition of fibrinolytic processes by antiphospholipid antibodies (aPLs) via cell surface receptors, including toll-like receptors (TLRs) [5,8]. Toll-like receptors (TLRs) are members of the pattern recognition receptor (PRR) family and play crucial functions in the innate immune system.…”