Immuno-regulatory function of indoleamine 2,3 dioxygenase through modulation of innate immune responses.

ABSTRACT: Successful long-term treatment of type-1 diabetes mainly relies on replacement of β-cells via islet transplantation. Donor shortage is one of the main obstacles preventing transplantation from becoming the treatment of choice. Although animal organs could be an alternative source for transplantation, common immunosuppressive treatments demonstrate low efficacy in preventing xenorejection. Immunoprotective effects of indoleamine 2,3-dioxygenase (IDO) on T-cell mediated allorejection has been extensively studied. Our studies revealed that IDO expression by fibroblasts, induced apoptosis in T-cells while not affecting non-immune cell survival/function. Since macrophages play a pivotal role in xenograft rejection, herein we investigated the effect of IDO-induced tryptophan deficiency/kynurenin

SUBMITTER: Poormasjedi-Meibod MS 

PROVIDER: S-EPMC3733714 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature