To determine whether the prolonged allograft survival was associated with enhanced autophagy, we examined the levels of autophagy-related protein beclin-1, microtubule associated pro-tein1 light chain 3 (LC3) I and II by Western blot analysis. As shown in Fig. 6A , only low levels of Beclin-1 and LC3 II were detected in control mice (rGST, untreated and PBS groups), but higher levels of Beclin-1 and LC3 II were observed in mice treated with Flt3L or Rapa alone. Importantly, the highest Beclin-1 and LC3 II expressions were noted in Flt3L/Rapa treated mice. To further confirm these results, we did immunohistochemical analysis, and similar results were obtained (Fig. 6A ). To examine the functional relevance for the enhanced autophagy in allograft survival, we performed similar transplantation along with the administration of 3-MA, an autophagy inhibitor [19, 20] . As expected, administration of 3-MA significantly repressed autophagy as determined by Western blot and immunohitochemical analysis (Fig. 6B) . Remarkably, repression of autophagy significantly attenuated Flt3L/Rapa therapy mediated protection against allograft rejection (Fig. 6C ). In consistent with this result, we also observed a decrease for the number of regulatory T cells and regulatory DCs (Fig. 6D) . Taken together, these data indicate that autophagy plays an essential role in Flt3L/Rapa therapy mediated protection against allograft rejection.