作者: Ari M. Mackler , Ellen M. Barber , Osamu Takikawa , Jeffrey W. Pollard
DOI: 10.4049/JIMMUNOL.170.2.823
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摘要: The tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) is expressed in macrophages that have been differentiated the presence of CSF-1 and important containment intracellular pathogens. IDO also appears to play a role suppression T cell responses variety contexts. In placenta, its enzymatic activity believed establish chemical barrier protects fetal allograft from cell-mediated immune aggression. We studied regulation utero-placental unit mice following infection with Gram-positive, bacterium Listeria monocytogenes has predilection for replication decidua basalis. mRNA protein expression enhanced L. monocytogenes. However, contrast human where by CSF-1R-positive syncytial trophoblast, not murine trophoblastic tissue but instead found stromal cells basalis metrial gland infection, endothelial cells. Using carrying null mutations cytokine/growth factor genes, we explored placenta. Consistent absence CSF-1R IDO-expressing mice, neither basal levels nor induction affected CSF-1. although level normal, during Listeriosis completely abrogated IFN-gamma, cytokine required resolution this infection. These data suggest plays resolving bacterial placenta while at same time maintaining whose might result rejection.