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Dendritic cells ( DC ) play a key role in the initiation of both antitumor immunity and immunological tolerance. It has been demonstrated that exposure to soluble factors produced by tumor cells modulates  DC  functions and induces tolerogenic  DC  differentiation. In this study, we investigated the effects of neuroblastoma cell line‐derived soluble factors on  DC  differentiation. Monocytes isolated from healthy volunteers were incubated with interleukin ( IL )‐4 and granulocyte‐macrophage colony‐stimulating factor in the presence of culture supernatants from neuroblastoma cell lines. The culture supernatants from neuroblastoma cell lines, such as  NLF  and  GOTO , partially blocked both downregulation of  CD 14 and upregulation of  CD 1a, and dramatically decreased  IL ‐12 and tumor necrosis factor ( TNF )‐α production from mature  DC , while no effect of  SH ‐ SY 5Y cell supernatant was noted. In addition,  IL ‐6 and  IL ‐10 production from monocytes was increased by the supernatants of  NLF  and  GOTO  cells at 24 hours after incubation. Furthermore, we evaluated  DC  functions through stimulation of invariant natural killer T ( iNKT ) cells. α‐Galactosylceramide‐pulsed  DC  co‐cultured with supernatants of  NLF  cells were unable to sufficiently stimulate  iNKT  cells. The decreased ability of  iNKT  cells to produce interferon ( IFN )‐γ after stimulation with neuroblastoma cell line supernatant‐cultured  DC  was reversed by addition of  IL ‐12.  CD 40 expression and  IL ‐12 production in  NLF ‐sup‐treated  DC  were increased by addition of exogenous  IFN ‐γ. These results indicate that tolerogenic  DC  are induced in the neuroblastoma tumor microenvironment and attenuate the antitumor effects of  iNKT  cells. Interactions between  iNKT  cells and αGalCer‐pulsed  DC  have the potential to restore the immunosuppression of tolerogenic  DC  through  IFN ‐γ production.

Soluble factors derived from neuroblastoma cell lines suppress dendritic cell differentiation and activation