Figure 12.
PTGS2highFCGR3− NK cells accelerate the growth of ectopic lesion and progression of EMS. (a,b) The expression of IL10 and TGFB in PTGS2+ FCGR3− NK cells and PTGS2− FCGR3+ NK cells in PF from patients with EMS (stage III and IV) (n = 10) was analyzed by FCM (Student t test). (c,d) The NK cells from WT, fcgr3−/- or ptgs2−/- mice were cocultured with mouse uterus stromal cells (USCs) for 48 h, and then the viability and apoptosis of USCs in vitro were analyzed by CCK8 assay (c) and apoptosis assay (d) (one-way ANOVA). (e) Immunohistochemistry analysis for the expression of BIRC5/survivin and PCNA in EMS-like lesions, in the EMS mouse model treated with vehicle, anti-FCGR3 (0.25 mg/kg/d) or celecoxib (5 mg/kg/d) (n = 6 mice/group). Original magnification: × 200. (f,g) The weight of EMS-like lesions in the EMS mouse model treated with vehicle, anti-FCGR3 or celecoxib (n = 6 mice/group) (one-way ANOVA). (h,i) The weight of EMS-like lesions in the NK-depleted EMS mouse model (anti-NK1.1 antibodies on days 0 and 3) treated with NK cells (day 5) from WT or ptgs2−/- mice (n = 8 mice/group) (Student t test). Data are expressed as the mean± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001.