Inhibition of indoleamine 2,3-dioxygenase, an immunoregulatory target of the cancer suppression gene Bin1, potentiates cancer chemotherapy

By A. Muller, J. DuHadaway, P. S. Donover, E. Sutanto‐Ward, George C. Prendergast. Nature Medicine, 2005

1,068 citations recorded by the source corpus.

Subfields: Biological Psychiatry, Molecular Biology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/bbe20ef5e449caa65685d4c55b19c71c219420f0

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Citations in the corpus

The Combined Effects of Tryptophan Starvation and Tryptophan Catabolites Down-Regulate T Cell Receptor ζ-Chain and Induce a Regulatory Phenotype in Naive T Cells1 (2006, background): “Discussion The immunosuppressive pathway of tryptophan catabolism has been implicated, with either protective or disease-promoting roles, in a variety of physiopathologic conditions, ranging from pregnancy (3) to transplantation (4), from autoimmunity (5) and inflammation (6, 7, 46) to neoplasia (11”
Impact of the Gut Microbiota on Intestinal Immunity Mediated by Tryptophan Metabolism (2018, background): “activity can directly enhance the immune capacity of tumorbearing mice against the tumors (Uyttenhove et al., 2003; Muller et al., 2005).”
Tryptophan catabolism in cancer: beyond IDO and tryptophan depletion. (2012, background): “tumor-suppressive effect of IDOorTDO inhibition is abrogated in immunodeficient hosts (11, 27, 28).”
Plasmacytoid dendritic cells from mouse tumor-draining lymph nodes directly activate mature Tregs via indoleamine 2,3-dioxygenase. (2007, background): “Transfection of IDO into tumor cells protects them from immune-mediated rejection (5), while inhibiting IDO in tumor-bearing hosts allows conventional chemotherapy to disrupt tolerance toward established tumors and trigger anti-tumor immune responses (6, 7).”
Understanding the intersections between metabolism and cancer biology (2017, neutral): “…both the innate and adaptive immune system and has been implicated in cancer-associated immunosuppression (Platten et al., 2014) and indoleamine-2,3-dioxygenase (IDO) inhibitors that decrease tryptophan metabolism can help break immune tolerance and potentiate chemotherapy (Muller et al., 2005).”
The Yin‐Yang of tumor‐associated macrophages in neoplastic progression and immune surveillance (2008, background): “By crossing HPV transgenic mice with severely immunodeficient recombination-activating gene-1 mice, it was found that genetic elimination of T and B lymphocytes blocks recruitment of innate immunity cells, tissue remodeling, and angiogenesis, with an arrest of the carcinogenesis process at the stage”
Role of tumor-associated macrophages in tumor progression and invasion (2006, background): “It was recently reported that the BAR adapterencoding gene Bin-1 inhibits IDO expression in cancer cells and macrophages and that inhibitors of IDO, such as methyl-thiohydantoin-tryptophan (MTH-trp), cooperate with cytotoxic agents to elicit regression of established tumors [84].”
Immunosuppressive strategies that are mediated by tumor cells. (2007, methodology): “Using a mouse knockout model, the authors showed that Bin1 can restrain immune escape of oncogenically-transformed cells by restricting expression of IDO (99).”
IDO in the Tumor Microenvironment: Inflammation, Counter-regulation and Tolerance (2016, positive): “Thus, when IDO is genetically deleted or pharmacologically inhibited, mice experience defects in creating tolerance to the fetus during allogeneic pregnancy [1-3], mucosal tolerance [4, 5], tolerance to apoptotic cells [6, 7] and other forms of acquired peripheral tolerance [8-13].”
Indoleamine 2,3-dioxygenase is a critical resistance mechanism in antitumor T cell immunotherapy targeting CTLA-4 (2013, methodology): “In addition to being constitutively expressed by many malignant cells (Muller et al., 2005a), IDO can be induced in tumor cells and APCs by proinflammatory stimuli such as IFN-, which is generated by the host immune response against the tumor (Taylor and Feng, 1991; Belladonna et al., 2009).”