Tolerance induction by antigen targeting to DNGR-1 could be useful in clinical settings for inducing transplantation tolerance or controlling autoimmunity and could be improved, for example, by co-administering immunomodulatory molecules, such as IL-2 and rapamycin, which expand freshly generated Treg while selectively dampening down the “effector” population 33. Here, IL2 is linked to Autoimmunity.