Fig. 5

hBMSCs or IL-6 promoted the growth of DLBCL cells by protecting them from spontaneous or drug-induced apoptosis, and IL-17A reinforced these effects. a Graphs of cell proliferation (OD) in 72-h cultures of SU-DHL-4 cells with or without hBMSCs (1:1), exogenous IL-6 (0.5 ng/ml), IL-17A (0.1 ng/ml), aIL-6 (50 μg/ml) and/or aIL-17A (10 μg/ml). b and c Apoptosis induced by rituximab (10 μg/ml) was protected by IL-6 or IL-17A. DLBCL cell cultures were first treated with exogenous IL-6 (0-5000 pg/ml) or IL-17A (0-5000 pg/ml), and rituximab was added 24 h before apoptosis detection. d Percentages of apoptotic SU-DHL-2 cells in 72-h cultures in the presence of rituximab (10 μg/ml), doxorubicin (2 μM) and Ara-C (2 μM). SU-DHL-2 cells were pre-cultured with exogenous IL-6 (0.5 ng/ml) and IL-17A (0.1 ng/ml) for 48 h before addition of drugs (rituximab, doxorubicin and Ara-C). e and f The sum of apoptotic SU-DHL-4 cell percentages induced spontaneously or by rituximab (10 μg/ml) in all groups. The culture conditions were the same as those in (a). g Representative FACS dot plots of apoptotic SU-DHL-4 cell percentages induced spontaneously or by rituximab (10 μg/ml) in all groups. The data shown represent one of three independent experiments. Error bars represent SD. Significance was determined using one-way ANOVA. (*P < 0.05; **P < 0.01)