The transcripts identified in this study are likely to be influenced by gestational age or disease status, or even play a direct role in the development of PE. In spite of several attempts during last decades to overcome the xenotransplant hyper acute rejection Epimedoside-A mediated by pre-formed antiaGal xeno-reactive antibodies, delayed xenograft rejection, mediated by progressive mononuclear cell infiltration, is still the main issue in preventing the widespread usage of animal organs for transplantation. Histopathological studies revealed a significant difference between mechanisms involved in cell mediated allogeneic and xenogeneic graft rejection. The main infiltrating cells in allograft rejection are TCR a/b positive cytotoxic T cells; while, xenografts are mainly infiltrated by NK cells and macrophages. Fox et al. study revealed that recognition of xenograft pathogen-associated molecular patterns by innate immune receptors leads to macrophage infiltration into the graft. The subsequent rapid and local innate immune response stimulates T cell infiltration. Infiltrated T cell subsequently activates macrophages to act as direct effector cells in xenograft rejection. Activated macrophages destruct the graft via secreting various proinflammatory mediators including TNF-a, reactive oxygen and nitrogen species, and complement factors. The difference between immune responses involved in allo- and xenogeneic graft rejection could explain why the routine immunosuppressive strategies are ineffective in supporting xenograft against immune rejection. Recent studies demonstrate that localized expression of immuno-regulatory factors, providing an immunoprivileged microenvironment, can be used as a feasible immunosuppressive strategy in post transplant patients. Indoleamine 2,3-dioxygenase, a cytosolic, heme containing enzyme, catalyses the first and rate-limiting step in metabolism of Pancuronium dibromide essential amino acid Ltryptophan to N-formylkynurenine. The immuno-regulatory function of IDO was first described regarding its role in preventing T cell-mediated allogeneic fetus rejection in mice. Further studies demonstrated the pivotal role of IDO in immunoregulation of cancer, inflammation and allergy, autoimmune disorders, and allotransplantation. Both local tryptophan deprivation and formation of toxic tryptophan catabolites contribute to immunosuppressive effects of IDO. The immuno-regulatory effects of IDO are mainly mediated through inhibition of T-cell proliferation, prevention of memory Tcells formation and induction of T-regulatory cells differentiation. We have previously shown that IDO-expressing fibroblast coculture with different subsets of primary human T cells leads to a significant reduction in T cell proliferation and survival. Forouzandeh et al. studies also revealed that selective activation of GCN2 kinase pathway in response to IDO induced tryptophan deficiency is responsible for T cell apoptosis. Further studies by our group demonstrated that IDO expression by bystander fibroblasts can prevent cellular and humoral alloimmune responses against islet allotransplant without having any adverse effect on viability and functionality of the graft. Although these data support the feasibility of using local IDO expression as an alternative for systemic immunosuppressive treatments following allotransplantation, there are limited reports that have examined the use of IDO expression for graft protection following xenotransplantation. Li et al. study demonstrated a significant reduction in the CD3 + T lymphocytes infiltration into the IDO expressing skin xenograft compared to control.