Reversal of IDO-mediated cancer immune suppression by systemic kynurenine depletion with a therapeutic enzyme

[1]  K. Satyshur,et al.  Trace derivatives of kynurenine potently activate the aryl hydrocarbon receptor (AHR) , 2017, The Journal of Biological Chemistry.

[2]  Lijun Sun,et al.  Targeting the IDO1/TDO2-KYN-AhR Pathway for Cancer Immunotherapy - Challenges and Opportunities. , 2017, Trends in pharmacological sciences.

[3]  G. Prendergast,et al.  Discovery of IDO1 Inhibitors: From Bench to Bedside. , 2017, Cancer research.

[4]  J. Ruas,et al.  Kynurenines: Tryptophan’s metabolites in exercise, inflammation, and mental health , 2017, Science.

[5]  C. Tomlinson,et al.  Indoleamine 2,3‐dioxygenase 1 (IDO1) inhibitors activate the aryl hydrocarbon receptor , 2017, Toxicology and applied pharmacology.

[6]  S. Bicciato,et al.  A Relay Pathway between Arginine and Tryptophan Metabolism Confers Immunosuppressive Properties on Dendritic Cells , 2017, Immunity.

[7]  C. Hopf,et al.  The stress kinase GCN2 does not mediate suppression of antitumor T cell responses by tryptophan catabolism in experimental melanomas , 2016, Oncoimmunology.

[8]  P. Thomas,et al.  Stress Kinase GCN2 Controls the Proliferative Fitness and Trafficking of Cytotoxic T Cells Independent of Environmental Amino Acid Sensing. , 2016, Cell reports.

[9]  J. Moffett,et al.  The end of the road for the tryptophan depletion concept in pregnancy and infection , 2016, Clinical science.

[10]  J. Wolchok,et al.  Targeting myeloid-derived suppressor cells with colony stimulating factor-1 receptor blockade can reverse immune resistance to immunotherapy in indoleamine 2,3-dioxygenase-expressing tumors , 2016, EBioMedicine.

[11]  D. Fuchs,et al.  IDO1 suppresses inhibitor development in hemophilia A treated with factor VIII. , 2015, The Journal of clinical investigation.

[12]  H. Heslop,et al.  Tumor indoleamine 2,3-dioxygenase (IDO) inhibits CD19-CAR T cells and is downregulated by lymphodepleting drugs. , 2015, Blood.

[13]  G. Prendergast,et al.  Accumulation of an Endogenous Tryptophan-Derived Metabolite in Colorectal and Breast Cancers , 2015, PloS one.

[14]  Y. Cheng,et al.  Durable Therapeutic Efficacy Utilizing Combinatorial Blockade against IDO, CTLA-4, and PD-L1 in Mice with Brain Tumors , 2014, Clinical Cancer Research.

[15]  H. Koblish,et al.  Mechanism of tumor rejection with doublets of CTLA-4, PD-1/PD-L1, or IDO blockade involves restored IL-2 production and proliferation of CD8+ T cells directly within the tumor microenvironment , 2014, Journal of Immunotherapy for Cancer.

[16]  R. Phillips.  Structure and mechanism of kynureninase. , 2014, Archives of biochemistry and biophysics.

[17]  H. Ball,et al.  Indoleamine 2,3-dioxygenase 2 (IDO2) and the kynurenine pathway: characteristics and potential roles in health and disease , 2013, Amino Acids.

[18]  Jason B. Williams,et al.  Up-Regulation of PD-L1, IDO, and Tregs in the Melanoma Tumor Microenvironment Is Driven by CD8+ T Cells , 2013, Science Translational Medicine.

[19]  R. Newberry,et al.  IDO1 metabolites activate β-catenin signaling to promote cancer cell proliferation and colon tumorigenesis in mice. , 2013, Gastroenterology.

[20]  J. Wolchok,et al.  Indoleamine 2,3-dioxygenase is a critical resistance mechanism in antitumor T cell immunotherapy targeting CTLA-4 , 2013, The Journal of experimental medicine.

[21]  S. Vollset,et al.  A community‐based study on determinants of circulating markers of cellular immune activation and kynurenines: the Hordaland Health Study , 2013, Clinical and experimental immunology.

[22]  J. Toldi,et al.  Kynurenines in the CNS: recent advances and new questions , 2012, Nature Reviews Drug Discovery.

[23]  W. Wick,et al.  Tryptophan catabolism in cancer: beyond IDO and tryptophan depletion. , 2012, Cancer research.

[24]  E. Gorelik,et al.  Immunological and Nonimmunological Effects of Indoleamine 2,3-Dioxygenase on Breast Tumor Growth and Spontaneous Metastasis Formation , 2012, Clinical & developmental immunology.

[25]  G. Georgiou,et al.  Strategies for optimizing the serum persistence of engineered human arginase I for cancer therapy. , 2012, Journal of controlled release : official journal of the Controlled Release Society.

[26]  M. Weller,et al.  An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor , 2011, Nature.

[27]  King-Thom Chung,et al.  Possible roles of excess tryptophan metabolites in cancer , 2011, Environmental and molecular mutagenesis.

[28]  J. Fechner,et al.  An Interaction between Kynurenine and the Aryl Hydrocarbon Receptor Can Generate Regulatory T Cells , 2010, The Journal of Immunology.

[29]  L. Raez,et al.  Tumor immunogenicity and responsiveness to cancer vaccine therapy: the state of the art. , 2010, Seminars in immunology.

[30]  Zlatko Trajanoski,et al.  In situ cytotoxic and memory T cells predict outcome in patients with early-stage colorectal cancer. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[31]  J. Wolchok,et al.  CTLA-4 blockade enhances polyfunctional NY-ESO-1 specific T cell responses in metastatic melanoma patients with clinical benefit , 2008, Proceedings of the National Academy of Sciences.

[32]  G. Prendergast,et al.  A key in vivo antitumor mechanism of action of natural product-based brassinins is inhibition of indoleamine 2,3-dioxygenase , 2008, Oncogene.

[33]  D. Munn,et al.  Indoleamine 2,3-dioxygenase and tumor-induced tolerance. , 2007, The Journal of clinical investigation.

[34]  G. Prendergast,et al.  Inhibition of indoleamine 2,3-dioxygenase in dendritic cells by stereoisomers of 1-methyl-tryptophan correlates with antitumor responses. , 2007, Cancer research.

[35]  Gerhard Opelz,et al.  Inhibition of Allogeneic T Cell Proliferation by Indoleamine 2,3-Dioxygenase–expressing Dendritic Cells , 2002, The Journal of experimental medicine.

[36]  G. Damonte,et al.  Tryptophan-derived Catabolites Are Responsible for Inhibition of T and Natural Killer Cell Proliferation Induced by Indoleamine 2,3-Dioxygenase , 2002, The Journal of experimental medicine.

[37]  R. McGraw,et al.  Cloning, sequence, and expression of kynureninase from Pseudomonas fluorescens. , 1997, Archives of biochemistry and biophysics.

[38]  J. Walker,et al.  Over-production of proteins in Escherichia coli: mutant hosts that allow synthesis of some membrane proteins and globular proteins at high levels. , 1996, Journal of molecular biology.

[39]  M. Jure-Kunkel,et al.  CTLA-4 blockade in tumor models: an overview of preclinical and translational research. , 2013, Cancer immunity.

[40]  S. Giordano,et al.  ReviewMolecular mechanisms of acquired resistance to tyrosine kinase targeted therapy , 2015 .

[41]  L. Trümper.  From bench to bedside , 2005, Medizinische Klinik.

[42]  Markus Voelter,et al.  State of the Art , 1997, Pediatric Research.