Indoleamine 2,3-dioxygenase (IDO) is an enzyme that catalyzes the catabolism of tryptophan, an essential amino acid, and is expressed in various cells, including antigen-presenting cells and the placenta. IDO expression in antigen-presenting cells has been shown to suppress allogeneic T cell proliferation by degrading tryptophan and producing metabolites such as kynurenine, which inhibit T cell function. In this study, human IDO gene was inserted into an adenoviral vector and expressed in dendritic cells (DCs), which then reduced tryptophan levels, increased kynurenine levels, and suppressed allogeneic T cell proliferation in vitro. Kynurenine, 3-hydroxykynurenine, and 3-hydroxyanthranilic acid were found to suppress T cell responses, with their effects being additive. T cells that had been suppressed could not be restimulated, suggesting that the suppression was due to T cell death. The tryptophan metabolites also affected B and NK cells but not DCs. These findings suggest that IDO-expressing DCs mediate immunosuppression through tryptophan metabolites, which may play a role in protecting the fetus during pregnancy and in T cell death in HIV-infected patients. The study highlights the role of IDO in immunosuppression and immunoregulation, and suggests that tryptophan metabolites may be involved in the pathogenesis of certain diseases. The results also indicate that IDO-expressing DCs could be used for inducing tolerance in transplant recipients.Indoleamine 2,3-dioxygenase (IDO) is an enzyme that catalyzes the catabolism of tryptophan, an essential amino acid, and is expressed in various cells, including antigen-presenting cells and the placenta. IDO expression in antigen-presenting cells has been shown to suppress allogeneic T cell proliferation by degrading tryptophan and producing metabolites such as kynurenine, which inhibit T cell function. In this study, human IDO gene was inserted into an adenoviral vector and expressed in dendritic cells (DCs), which then reduced tryptophan levels, increased kynurenine levels, and suppressed allogeneic T cell proliferation in vitro. Kynurenine, 3-hydroxykynurenine, and 3-hydroxyanthranilic acid were found to suppress T cell responses, with their effects being additive. T cells that had been suppressed could not be restimulated, suggesting that the suppression was due to T cell death. The tryptophan metabolites also affected B and NK cells but not DCs. These findings suggest that IDO-expressing DCs mediate immunosuppression through tryptophan metabolites, which may play a role in protecting the fetus during pregnancy and in T cell death in HIV-infected patients. The study highlights the role of IDO in immunosuppression and immunoregulation, and suggests that tryptophan metabolites may be involved in the pathogenesis of certain diseases. The results also indicate that IDO-expressing DCs could be used for inducing tolerance in transplant recipients.