Fig. 5

HMGB1 promoted the secretion of CXCL11. a Representative immunostaining using anti-HMGB1 and anti-CXCL11 mAbs in serial sections from 2 different patients. Preferential expressions of HMGB1 with CXCL11 in lung cancers (n = 100) was analyzed as shown. Figure panel pairs represents images taken with different zooming options; scale bars, 100 μm. b, c CXCL11 RNA and protein levels in A549 cells after treatment with different doses of rHMGB1 for 24 h, as assayed by qRT-PCR and ELISA. Statistical differences between groups were determined by the Student t test. *P < 0.05; **p < 0.0001. d, e The release of CXCL11 in A549 cells after treatment with rHMGB1 at different time points was determined by qRT-PCR and ELISA. Statistical differences between groups were determined by the Student t test. *P < 0.05; **P < 0.0001. f HMGB1 protein levels in A549 cells after incubation with siRNA. g, h When HMGB1 transcription was silenced using siRNA, DOC selectively failed to induce HMGB1 and CXCL11 in A549 cells. Data are given as means ± SEM. *P < 0.05; **P < 0.0001. Experiments were independently repeated three times. i The relative mRNA levels of CD8, Perforin, Granzyme B and IFN- γ were analyzed in primary tumors secreting high levels (n = 50) or low levels of HMGB1 (n = 50). Data are given as means ± SEM. *, P < 0.05; **, P < 0.0001