Richard P. Metz

TL;DR: It was found that a first exposure of mice to LPS activated the ligand-operated transcription factor aryl hydrocarbon receptor and the hepatic enzyme tryptophan 2,3-dioxygenase, which provided an activating ligand to the former, to downregulate early inflammatory gene expression, pointing to a role for AhR in contributing to host fitness.

TL;DR: A personal perspective on IDO as a nodal mediator of pathogenic inflammation and immune escape in cancer is provided to provide a conceptual foundation for the clinical development of IDO inhibitors as a novel class of immunomodulators with broad application in the treatment of advanced human cancer.

TL;DR: This study provides preclinical, genetic proof-of-concept that the immunoregulatory enzyme IDO contributes to autochthonous carcinoma progression and to the creation of a metastatic niche.

TL;DR: It is suggested that the mammary gland microenvironment becomes promotional for tumor cell dissemination during involution, thus providing a plausible mechanism to explain the high rate of metastases that occur with pregnancy-associated breast cancer.

TL;DR: These results offer an initial glimpse into immune modulation by IDO2, revealing its genetic interaction with IDO1 and distinguishing its non-redundant contributions to inflammation, and establishing a functional role for Ido2 in immune modulation.