Immunosuppressive Role of Myeloid-Derived Suppressor Cells and Therapeutic Targeting in Lung Cancer

Figure 1

Targeting MDSCs in the treatment of lung cancer. Retinoic acid can stimulate the differentiation of myeloid progenitor cells to dendritic cells or macrophages, thereby inhibiting the differentiation of MDSCs. c-KIT can inhibit the signaling pathway which is mediated by SCF, inhibiting the amplification of MDSCs. The inhibition of COX2 expression in MDSCs can decrease the release of arginine-1, Nrf2 contributes to the clearance of ROS in MDSCs, and both COX2 and Nrf2 can inhibit the function of MDSCs. The above measures will inhibit MDSCs’ immunosuppressive function on effector T cells and enhance the antitumor immunity. SCF: stem cell factor; VEGF: vascular endothelial growth factor; COX2: cyclooxygenase 2; Arg-1: arginine-1; Nrf2: nuclear factor erythroid 2 p45-related factor 2; ROS: reactive oxygen species; CTL: cytotoxic lymphocyte.