Statement of the ProblemWe recently established a novel method for the genetic modification of Dendritic cell (DC). In the method, we generated DC from mouse embryonic stem (ES) cells by in vitro differentiation. The capacity of ES cell-derived DC (ES-DC) to simulate T cells was comparable to that of DC generated in vitro from Bone marrow (BM) cells (BMDC). On the other hand, in the future clinical application of this technology, we will face the problem of histoincompatibility between patients to be treated and the ES cells as source of DC. In the present study, we tested whether the transferred semi-allogeneic ES-DC can activate antigen-specific CTL restricted to the shared MHC class I molecules before they are eliminated by allo-reactive CTL.Materials and MethodsWe adoptively transferred OVA-expressing ES-DC to semi-allogeneic mice and examined whether or not they could activate OVA-specific CTL restricted to the shared MHC class I and elicit protective immunity against tumor cells expressing OVA.Method of Data AnalysisWe used Chromium release assay for detection of CTL activity.And in vivo cancer prevention assay was evaluated by tumor index and survival rate.ResultsWe observed that OVA-expressing ES-DC transferred into semi-allogeneic mice potently primed OVA-specific CTL restricted to the shared MHC class I and elicited a significant protection against challenge with OVA-expressing tumor.ConclusionThese results suggest the potential of ES-DC as a novel means for anti-cancer immunotherapy. Statement of the ProblemWe recently established a novel method for the genetic modification of Dendritic cell (DC). In the method, we generated DC from mouse embryonic stem (ES) cells by in vitro differentiation. The capacity of ES cell-derived DC (ES-DC) to simulate T cells was comparable to that of DC generated in vitro from Bone marrow (BM) cells (BMDC). On the other hand, in the future clinical application of this technology, we will face the problem of histoincompatibility between patients to be treated and the ES cells as source of DC. In the present study, we tested whether the transferred semi-allogeneic ES-DC can activate antigen-specific CTL restricted to the shared MHC class I molecules before they are eliminated by allo-reactive CTL. We recently established a novel method for the genetic modification of Dendritic cell (DC). In the method, we generated DC from mouse embryonic stem (ES) cells by in vitro differentiation. The capacity of ES cell-derived DC (ES-DC) to simulate T cells was comparable to that of DC generated in vitro from Bone marrow (BM) cells (BMDC). On the other hand, in the future clinical application of this technology, we will face the problem of histoincompatibility between patients to be treated and the ES cells as source of DC. In the present study, we tested whether the transferred semi-allogeneic ES-DC can activate antigen-specific CTL restricted to the shared MHC class I molecules before they are eliminated by allo-reactive CTL. Materials and MethodsWe adoptively transferred OVA-expressing ES-DC to semi-allogeneic mice and examined whether or not they could activate OVA-specific CTL restricted to the shared MHC class I and elicit protective immunity against tumor cells expressing OVA. We adoptively transferred OVA-expressing ES-DC to semi-allogeneic mice and examined whether or not they could activate OVA-specific CTL restricted to the shared MHC class I and elicit protective immunity against tumor cells expressing OVA. Method of Data AnalysisWe used Chromium release assay for detection of CTL activity.And in vivo cancer prevention assay was evaluated by tumor index and survival rate. We used Chromium release assay for detection of CTL activity.And in vivo cancer prevention assay was evaluated by tumor index and survival rate. ResultsWe observed that OVA-expressing ES-DC transferred into semi-allogeneic mice potently primed OVA-specific CTL restricted to the shared MHC class I and elicited a significant protection against challenge with OVA-expressing tumor. We observed that OVA-expressing ES-DC transferred into semi-allogeneic mice potently primed OVA-specific CTL restricted to the shared MHC class I and elicited a significant protection against challenge with OVA-expressing tumor. ConclusionThese results suggest the potential of ES-DC as a novel means for anti-cancer immunotherapy. These results suggest the potential of ES-DC as a novel means for anti-cancer immunotherapy.