Fig. 7

CXCL1/CXCR2 signaling regulates the proliferation, motility, and immunosuppressive activity of spleen-derived MDSCs. A MDSCs proliferation under different treatments for 24 h was determined by EdU assay. MDSCs motility was assessed using the Transwell chamber. B Proliferation and motility of spleen-derived MDSCs from CXCR2 knockout mice (CXCR2^KO) or CXCR2 wild-type mice (CXCR2^WT) were detected with or without CXCL1 (10 ng/ml) treatment for 24 h. C The proliferation of CD8⁺ T cells in the MDSCs (from CXCR2^WT or CXCR2^KO mice) co-culture system was detected by CFSE assay. D-E The granzyme B and perforin levels were measured in the MDSCs (from CXCR2^WT or CXCR2^KO mice) and CD8⁺ T cells co-culture system. F MDSCs were untreated or pretreated with CXCL1 (10 ng/ml) for 24 h. The capability of MDSCs to induce 4T1 migration was detected in the transwell co-culture system. G Flow diagram for 4T1 cell apoptosis detection (upper panel). MDSCs were untreated or pretreated with CXCL1 (10 ng/ml) for 24 h. MDSCs were then co-cultured with 4T1 and CD8⁺ T cells (CD8⁺T: MDSCs: 4T1 = 5: 2.5: 1) for 24 h. The 4T1 cells were collected and further distinguished by CD45⁻ gating. The ability of MDSCs inhibiting CD8⁺ T-induced apoptosis in 4T1 cells was measured using AnnexinV and 7-ADD labeling (lower panel). Data are represented as Mean ± SD. For statistical analysis, unpaired t-tests were applied. ^*P < 0.05, ^#P < 0.01