Engagement of the aryl hydrocarbon receptor in M. tuberculosis-infected macrophages has pleiotropic effects on innate immune signaling

ABSTRACT: Understanding the mechanisms of host macrophage responses to M. tuberculosis (M.tb.) is essential for uncovering potential avenues of intervention to boost host resistance to infection. Macrophage transcriptome profiling revealed M.tb. infection strongly induced expression of several enzymes controlling tryptophan (Trp) catabolism. This included indole 2,3-dioxygenase 1 (IDO1) and tryptophan 2,3-dioxygenase (TDO2), which catalyze the rate-limiting step in the kynurenine pathway, producing ligands for the aryl hydrocarbon receptor (AHR). The AHR and heterodimeric partners AHR nuclear translocator (ARNT) and RELB are robustly expressed, and AHR and RELB levels further increased during infection. Infection enhanced AHR/ARNT and AHR/RELB DNA binding, and stimulated expression of AHR target gen

ORGANISM(S): Homo sapiens

SUBMITTER: John White 

PROVIDER: E-GEOD-70200 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress