Induction of PD-1 in B cells by TLR agonists and primary HCC-SN.

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Presentation transcript:

Induction of PD-1 in B cells by TLR agonists and primary HCC-SN. Induction of PD-1 in B cells by TLR agonists and primary HCC-SN. A and B, culture supernatants from primary HCC cells (HCC1-SN and HCC2-SN), but not normal liver (Hem-liver-SN), induced PD-1+/hi B cells with CD5+CD27+ phenotype in healthy blood B cells. Results shown represent six separate experiments (N = 8). C, effects of HCC-SN and indicated cytokines (all 10 ng/mL) on PD-1 expression by B cells with or without CD40L (1 μg/mL) stimulation. D, IL4 abolished HCC-SN–mediated B-cell PD-1 upregulation. E, FACS analysis of PD-1 on B cells cultured in medium or stimulated with intermediate-HA fragments (50–200 kDa) at 5 μg/mL (HA-5) or 10 μg/mL (HA-10). F, blockade of TLR4 in B cells treated with HA and blocking HA with HA-specific blocking peptide Pep-1 in HCC-SN both significantly inhibited PD-1+ and PD-1hi B-cell generation. Pep-C, control peptide. G, blockade of TLR4 significantly inhibited PD-1+ and PD-1hi B-cell generation induced by primary HCC-SN. H and I, knockout of TLR4 (H) and injection of Pep-1 (I) effectively suppressed PD-1+ and PD-1hi B-cell generation in tumor-bearing C57BL/10 mice. Data are given as mean ± SEM (N = 10 each group). PD-1 expression on B cells was determined by FACS after incubation with the indicated stimuli for 3 days (A–G). Values in dashed boxes represent the percentages of PD-1hi B cells (A and E) or of CD5+PD-1hi or CD27+PD-1hi B cells (B). Results shown in C–G represent mean ± SEM of three or four independent experiments (N = 4–5). *, P < 0.05; **, P < 0.01; ***, P < 0.001 (Student t test). Xiao Xiao et al. Cancer Discov 2016;6:546-559 ©2016 by American Association for Cancer Research