Figure 1.

Molecular mechanisms of MDSCs on the immune system. Several mechanisms contribute to MDSC-induced immune suppression and hyperinflammatory activation in viral infection and including those with COVID-19 patients. Specially, MDSCs are able to suppress T cells, NK cells, and other myeloid cells function. T cells are mainly inhibited through the production of ROS or depletion of L-arginine, and the delayed production of IFN-1 seems to result in the continuous accumulation of MDSCs into the lungs. Several signaling pathways, such as STAT1/3/6, are involved, to increase levels of immunosuppressive factors such as ROS, iNOS, NO, and Arg-1, which inhibit T cell responses. High levels of PD-L1 found in MDSCs and macrophages can reduce the activation of antigen-specific T cells by binding to the PD-1 receptor on T cells. In addition, the release of IL-10 and TGF-β by MDSC induces additional inflammatory system of macrophages by recruiting lymphocytes and granulocytes as well as inflammatory monocytes. MDSCs, myeloid derived suppressor cells; NK, natural killer cell; ROS, reactive oxygen species; TGF-β, transforming growth factor-β; APC, antigen presenting cells; NO, nitric oxide; STAT, signal transducer and activator of transcription; JAK, janus activated kinase; IL, interleukin; MMP, matrix metalloporteinases; G-CSF, granulocyte colony stimulating factor; COX-2, cyclooxygenase 2; Arg, arginine.