Fig. 3

Blocking or activating LILRB4 could downregulate or upregulate the levels of p-SHP2, p-STAT6, Arg-1 and IL-10 in dMDSCs during T. gondii infection. a The expression levels of SHP-2, p-SHP2, STAT6, p-STAT6, Arg-1 and IL-10 in human dMDSCs treated with or without α-LILRB4 and APOE after infection with T. gondii were detected by Western blot. b–d The expression levels of p-SHP2, p-STAT6 and Arg-1 in mouse dMDSCs from the WT and LILRB4^−/− infected mice were detected by flow cytometry. The data on human dMDSCs were identified by a paired t-test. The data on mouse dMDSCs were identified by the unpaired t-test. Asterisks indicate a significant difference at *p < 0.05 and **p < 0.01. APOE, apolipoprotein E; Arg-1, arginase-1; FMO, fluorescence minus one; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; IL-10, interleukin-10; INF, infected; LILRB4-/-, LILRB4-deficient; p-SHP2, phosphorylated SHP-2; p-STAT6, phosphorylated STAT6; SHP-2, src-homology 2 domain-containing protein tyrosine phosphatase; STAT6, signal transducer and activator of transcription 6; WT, wild type; αLILRB4: anti-LILRB4-neutralized.