Table 4.

A schematic diagram of promising therapeutic roles of MDSCs in OS.

Study. (year). Ref	Source	Mechanism	Promising therapeutic target
Ligon et al.(2021) (94)	tissue from OS patients	Targeting MDSCs suppressing T-cell infiltration into the PM of OS to block OS metastasis	Gene regulation
Deng et al.(2020) (95)	80 OS patients from database and 27 OS patients	Neoadjuvant chemotherapy reduce the MDSCs number and convert OS into an immune “hot” tumor.	MDSCs’ reduction
Jiang et al.(2019) (96)	K7M2 mouse OS model	OS-infiltrating MDSCs were CXCR4 positive and would migrate toward an SDF-1 gradient. The axis of CXCR4/SDF-1 could reduce the apoptosis of MDSCs.	MDSCs’ apoptosis induction
Shi et al.(2019) (97)	K7M2 mouse OS model	Combining SNA with anti-PD1 regulated innate immune cells, slowed OS tumor growth and prolonged survival time of tumor-bearing mice via inhibiting the function of MDSCs with a selective PI3Kδ/γ inhibitor to enhance responses to immune checkpoint blockade.	Supplement classical immunotherapy
Uehara et al.(2019) (98)	K7M2neo OS model	Met regulated the metabolism of MDSCs to decrease OXPHOS and enhance glycolysis to inhibit OS growth.	MDSCs’ metabolism
Guan et al.(2017) (99)	Mouse tumor model	IL-18 inducing MDSC to infiltrate into the OS parenchyma	MDSCs’ migration
Long et al.(2016) (100)	NSG mice	ATRA treatment enhances efficacy of GD2-CAR T cells against OS by eradicating monocytic MDSCs and diminishing the suppressive capacity of granulocytic MDSCs.	MDSCs’ reduction