Table 3 MDSCs in leukemia and MDS

AML, n = 8

eMDSCs

CD11b + HLA-DR-CD33 + lin-

Higher MDSCs in PB and BM vs. healthy donor

MDSCs contribute to tumor-related immune suppression

MUC1 mediates MDSC expansion via the promotion of c-myc expression in secreted extracellular vesicles.

AML, n = 30

MDSCs

CD11b + HLA-DR-CD33+

Higher VISTA+ cells among MDSCs from AML patients vs. healthy controls

VISTA knockdown diminished the inhibition of CD8 T cell activity by MDSCs in AML

ALL-B, n = 43

G-MDSCs

HLA-DR^−/low CD11b + CD33^int/high

Higher MDSCs in PB and BM vs. healthy donor

B-ALL-derived G-MDSCs was mediated through the production of reactive oxygen species and required direct cell-cell contact, with the potential participation of STAT3 signaling.

APL, n = 31

M-MDSCs

CD33 + CD14 + HLA-DR-

Higher MDSCs in PB vs. healthy donor

ATRA treatment reverses the increase of ILC2-MDSC in APL

ILC2-derived IL-13 promotes functional M-MDSC

MDS, n = 12

MDSCs

Lin–HLA-DR–CD33+

Higher MDSCs in PB vs. healthy donor

Interaction of S100A9 with CD33 promoted MDSCs and induce secretion of IL-10 and TGF-β

Early forced maturation of MDSC rescued the hematologic phenotype

MDS, n = 40

eMDSCs

CD33(+)HLA-DR(−)Lin(−)

Activation of the CD33 pathway of MDSCs can cause reactive oxygen species (ROS)-induced genomic instability.

Fc-engineered monoclonal antibody against CD33 reduce MDSC, block CD33 downstream signaling preventing immune-suppressive cytokine secretion, and reduced both ROS and the levels of double strand breaks and adducts

CML, n = 36

MDSCs

CD11b + CD14 − CD33+

PB MDSC levels were increased in samples from Sokal high-risk patients

Arginase 1↑PD-L1/PD-1 on T cells↑

CML, n = 19

G-MDSCs

CD11b + CD33 + CD14-HLADR-

M-MDSCs CD14 + HLADR-

PB MDSC levels were increased at diagnosis and returned to normal after therapy

Higher Arg1 expression in MDSCs

CLL, n = 41

M-MDSCs

CD14 + HLA-DR^Low

Higher IDO^hi MDSCs in PB vs. healthy donor

CLL cells induce conversion of monocytes into M-MDSCs.