English: Treg migrate to the grafted tissue. Activated Treg convert ATP released by inflamed tissues to adenosine via the ectoenzymes CD39 and CD73. Local adenosine could contribute to the initial “privileged” microenvironment. Treg also secrete TGF-β and IL-10 which inhibit the maturation and migration of dendritic cells (DC). These “decommissioned” DC can secrete catabolic enzymes for depletion of essential amino acids (EAA) and, therefore, induce apoptosis of effector T cells. Moreover, the “privileged” tissues could release pro-apoptotic galectin-9 which binds to TIM-3 expressed by effector T cells such as Th1 and Th17. This further amplifies the immunosuppressive microenvironment. Each of these components within the graft can further reinforce the local anti-inflammatory state such that any naive T cell, migrating into this area, will be converted to induced Treg (iTreg) through infectious tolerance. The iTreg then expand and further suppress immunity in the “privileged” microenvironment.