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Infectious disease


Aryl hydrocarbon receptor (AHR); indoleamine 2,3-dioxygenase 1 (IDO1)

Mouse studies suggest stimulating IDO1 activity could help establish endotoxin tolerance in sepsis. In a mouse model of lipopolysaccharide (LPS)-induced sepsis, knocking out Ido1, which encodes an enzyme that produces Ahr ligands, prevented establishment of an endotoxin-tolerant state. In cultured mouse dendritic cells, genetic depletion of Ahr decreased Ido1 expression and Ido1 phosphorylation compared with no alteration, suggesting a feed-forward mechanism from Ahr to Ido1 after initial LPS exposure. Next steps include developing strategies to sustain IDO1 activity and characterizing specific interactions between AHR and the AHR ligand kynurenine.

SciBX 7(28); doi:10.1038/scibx.2014.830
Published online July 24, 2014

Patent application filed; available for licensing

Bessede, A. et al. Nature; published online July 9, 2014;
Contact: Paolo Puccetti, University of Perugia, Perugia, Italy
Contact: Francesca Fallarino, same affiliation as above