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Memory T cell responses develop following exposure to pathogen infection or inocuous agents such as transfused blood or fetal antigens.  Pre-established memory T cell responses have been demonstrated to inhibit the prolonged survival and tolerance of a transplanted graft.  A normal course of immunosuppression following transplantation increases the patients’  risk of exposure to not only new infections, but also reactivation of native infections, such as the prevalent herpes viruses EBV and CMV.  Novel infections and recurrent ones alike lead to increased rejection of the transplanted organ.  Current studies aim at understanding the effect of systemic pathogen infections on transplantation tolerance.  Specifically, we are investigating the effect of pathogen infection on regulatory T cell function and protection of the transplanted allograft.