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Summary  Cancer immunity is mediated through the effective priming and activation of tumour‐specific class I  MHC  molecule‐restricted  CD 8 +  cytotoxic T lymphocytes ( CTL s).  DEC ‐205 +  dendritic cells ( DC s) can cross‐present the epitope(s) of captured tumour antigens associated with class I  MHC  molecules alongside co‐stimulatory molecules to prime and activate tumour‐specific  CD 8 +   CTL s. Immunosuppressive tolerogenic  DC s with reduced co‐stimulatory molecules may be a cause of impaired  CTL  induction. Hepa1‐6‐1 cells were established from the mouse hepatoma cell line Hepa1‐6; these cells grow continuously after subcutaneous implantation into syngeneic C57 BL /6 (B6) mice and do not prime  CD 8 +   CTL s. In this study, we show that the growth of ongoing tumours was suppressed by activated  CD 8 +   CTL s with tumour‐specific cytotoxicity through the administration of the glycolipid  α ‐galactosylceramide ( α ‐GalCer), which is a compound known to stimulate invariant natural killer T ( iNKT ) cells and selectively activate  DEC ‐205 +   DC s. Moreover, we demonstrated that sequential repetitive intraperitoneal inoculation with  α ‐GalCer every 48 hr appeared to convert tolerogenic  DEC ‐205 +   DC s into immunogenic  DC s with a higher expression of co‐stimulatory molecules and a stronger cross‐presentation capacity, which primed  CTL  precursors and induced tumour‐specific  CD 8 +   CTL s within the tumour environment without activating  iNKT  cells. These findings provide a new basis for cancer immunotherapy to convert tolerogenic  DEC ‐205 +   DC s within tumours into immunogenic  DC s through the sequential administration of an immuno‐potent lipid/glycolipid, and then activated immunogenic  DC s with sufficient expression of co‐stimulatory molecules prime and activate tumour‐specific  CD 8 +   CTL s within the tumour to control tumour growth.

immunology

Suppression of murine tumour growth through  CD 8 +  cytotoxic  T  lymphocytes via activated  DEC ‐205 +  dendritic cells by sequential administration of  α ‐galactosylceramide  in vivo