Abstract: Deep vein thrombosis (DVT) is an abnormal formation of a blood clot within a deep vein, which causes blood flow back in the lumen to be blocked. DVT not only has high morbidity and mortality, but also has a high economic burden to patients. The pathogenesis is still unclear due to the absence of suitable DVT model. DVT has long been considered as a blood coagulation disorder. DVT prophylaxis focuses predominantly on the coagulation system, including thrombin (Dabigatran), active FXa (Rivaroxaban) or vitamin K-dependent clotting factors (Warfarin). Nevertheless, due to the mechanisms of normal hemostasis and pathological thrombosis are greatly overlapped, the therapeutic window of anticoagulants may be narrow because of increased risks for bleeding complications. Recently studies demonstrate that immune cells and cytokines are involved in DVT initiation, and may play a vital role in DVT. These studies consider DVT as an immunity- and inflammation-related process rather than merely coagulation-dependent thrombosis. Immune cells related to the formation of DVT include mast cells, neutrophils, monocytes, platelets, etc. The cytokines mainly include P-selectin, complement activator, cell adhesion molecule, interleukin, etc. Additionally, ROS and MRP-14 are all play an important role in DVT. Blood flow stagnation in the vein results in hypoxia, following with endothelial activation and recruitment of various immune cells, which leading to intravenous thrombosis. Inflammatory cytokines are involved in the processes, and they play a crucial role in DVT with immune cells. Now, we review the advance of research on various immune cells and cytokines in DVT, respectively.