First, we evaluated the qualities of the BMT model. Multilineage-full

chimerism in the case of BMT using fully allogeneic BMC and multilineage-mixed chimerism in the case of BMT using mixed BMC were confirmed in the PBL of all recipients prior to tumour inoculation (Fig. 4A and data not shown). As previously reported, a small population of recipient-derived radio-resistant T cells were detected in recipients transplanted with BL6 BMC (the lower right dot plot in Fig. 4A). However, these T cells showed no alloresponses [29] and so should not affect the survival time of injected allogeneic DC. The B-cell and myeloid lineage chimerism selleck kinase inhibitor in the PBL was complete in the recipients transplanted with BL6 BMC (the upper right dot plot in Fig. 4A and data not shown). This suggests that the bone marrow haematopoietic cells had been completely replaced by donor-derived BMC. We also assessed the chimerism of the DC in the lymph nodes (inguinal and axillary) and tumours of the B/c recipients. A significant Dabrafenib price percentage of recipient-derived DC was detected in the lymph nodes of recipients transplanted with BL6 BMC (Fig. 4B). More than 60% of residual B/c recipient-derived H-2Kd positive DC in the cutaneous draining lymph nodes expressed DEC205 and I-Ad high, both markers

found on Langerhans cells (data not shown) [34]. This suggests that these cells were derived from Langerhans cells repopulated from the radio-resistant progenitor cells in the cutaneous niche [35]. Because Langerhans progenitor cells in the cutaneous niche are destroyed by any contaminating donor-derived T cells

that mediate graft-versus-host disease (GVHD) [35], the presence of host-derived Langerhans cells in the draining lymph nodes in this study suggests that the T-cell depletion of the donor BMC was complete. This is supported by the fact that we observed no GVHD response in these mice; this observation was confirmed by histological analysis at autopsy (data not shown). To the contrary, almost all tumour-associated DC were positive for H-2Kb and negative for H-2Kd (Fig. 4B). This suggests that the tumour-associated DC were derived from donor BMC. Taken together, we judged that the developed BMT model was qualitatively appropriate to evaluate the three factors individually in ITADT. Surprisingly, we found that ITADT else using BL6 DC showed a significant antitumour effect in terms of tumour growth suppression as well as ITADT using B/c DC in recipients of mixed BMC (BL6+ B/c B/c), despite the MHC incompatibility of the injected BL6 DC (Fig. 4, middle graph). However, ITADT using BL6 DC did not show any significant antitumour effect in recipients of BL6 BMC, despite the fact that these recipients were tolerant to BL6 (Fig. 4, left-hand graph), while ITADT using B/c DC did show a significant antitumour effect in recipients of BL6 BMC. In recipients of syngeneic BMC (B/c B/c), ITADT using B/c DC showed a significant antitumour effect.