Inhibition of interferon-mediated induction of indoleamine 2,3-dioxygenase in mouse lung by inhibitors of prostaglandin biosynthesis.

Sayama, Shigetoshi; Yoshida, Ryotaro; Oku, Tohru; Imanishi, Jirô; Kíshida, Tsunataro; Hayaishi, Osamu

doi:10.1073/pnas.78.12.7327

Cited by 41 publications

(26 citation statements)

References 26 publications

(23 reference statements)

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“…For example, early studies in mouse lung slices treated with IFNγ reported that COX inhibitors (aspirin and indomethacin) inhibited IDO1 induction [97]. Subsequent studies indicate an important role for COX2-derived PGE 2 in elevating IDO1 in different tumour cells (e.g.…”

Section: Control Of Ido1 Gene Expressionmentioning

confidence: 98%

Role of indoleamine 2,3-dioxygenase in health and disease

et al. 2015

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IDO1 (indoleamine 2,3-dioxygenase 1) is a member of a unique class of mammalian haem dioxygenases that catalyse the oxidative catabolism of the least-abundant essential amino acid, L-Trp (L-tryptophan), along the kynurenine pathway. Significant increases in knowledge have been recently gained with respect to understanding the fundamental biochemistry of IDO1 including its catalytic reaction mechanism, the scope of enzyme reactions it catalyses, the biochemical mechanisms controlling IDO1 expression and enzyme activity, and the discovery of enzyme inhibitors. Major advances in understanding the roles of IDO1 in physiology and disease have also been realised. IDO1 is recognised as a prominent immune regulatory enzyme capable of modulating immune cell activation status and phenotype via several molecular mechanisms including enzyme-dependent deprivation of L-Trp and its conversion into the aryl hydrocarbon receptor ligand kynurenine and other bioactive kynurenine pathway metabolites, or non-enzymatic cell signalling actions involving tyrosine phosphorylation of IDO1. Through these different modes of biochemical signalling, IDO1 regulates certain physiological functions (e.g. pregnancy) and modulates the pathogenesis and severity of diverse conditions including chronic inflammation, infectious disease, allergic and autoimmune disorders, transplantation, neuropathology and cancer. In the present review, we detail the current understanding of IDO1's catalytic actions and the biochemical mechanisms regulating IDO1 expression and activity. We also discuss the biological functions of IDO1 with a focus on the enzyme's immune-modulatory function, its medical implications in diverse pathological settings and its utility as a therapeutic target.

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Section: Control Of Ido1 Gene Expressionmentioning

confidence: 98%

Role of indoleamine 2,3-dioxygenase in health and disease

et al. 2015

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“…207 Induction of IDO can also be blocked in vitro by cyclooxygenase 2 inhibitors. 212 When murine breast cancer vaccine recipients received the oral cyclooxygenase 2 inhibitor celecoxib, an increase in tumor-specific CTLs was observed. 35 Trophoblast invasion and spiral artery remodeling are tightly controlled processes, likely kept in check both by molecular programming of trophoblast cells and by paracrine immune factors.…”

mentioning

confidence: 99%

Cancer and Pregnancy: Parallels in Growth, Invasion, and Immune Modulation and Implications for Cancer Therapeutic Agents

Holtan

Creedon

Haluska

et al. 2009

Mayo Clinic Proceedings

252

179

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Many proliferative, invasive, and immune tolerance mechanisms that support normal human pregnancy are also exploited by malignancies to establish a nutrient supply and evade or edit the host immune response. In addition to the shared capacity for invading through normal tissues, both cancer cells and cells of the developing placenta create a microenvironment supportive of both immunologic privilege and angiogenesis. Systemic alterations in immunity are also detectable, particularly with respect to a helper T cell type 2 polarization evident in advanced cancers and midtrimester pregnancy. This review summarizes the similarities between growth and immune privilege in cancer and pregnancy and identifies areas for further investigation. Our PubMed search strategy included combinations of terms such as immune tolerance, pregnancy, cancer, cytokines, angiogenesis, and invasion. We did not place any restrictions on publication dates. The knowledge gained from analyzing similarities and differences between the physiologic state of pregnancy and the pathologic state of cancer could lead to identification of new potential targets for cancer therapeutic agents. © 2009 Mayo Foundation for Medical Education and ResearchA substantial body of literature exists describing the mechanisms cancer cells use to escape apoptosis and migrate through normal structures while evading a host immune response. What is not well known, however, is how these complex and interrelated mechanisms are orchestrated, starting with modulation of the immune response within the tumor microenvironment and ending with migration and proliferation of cancer cells at distant sites. One potential model to further study how a single malignant cell could proliferate and then metastasize undetected within a host is that of normal human pregnancy, in which the developing placenta invades the uterus and a semiallogeneic fetus escapes rejection from the maternal immune system. 1 A multitude of immunomodulatory properties of the fetomaternal interface (placenta) have evolved to allow the survival of the immunologically distinct fetus to parturition without an attack from the maternal immune system. The similarities between the mechanisms involved in fetomaternal and tumor-associated immunologic tolerance are intriguing and suggest a common pattern; however, neither system of immune evasion is perfect. A clear example of placental failure to protect the fetus against maternal immunity is that of Rh incompatibility. In multiparous women sensitized against fetal Rh antigens, re-exposure to fetal Rh antigens with subsequent pregnancy may lead to hemolytic disease of the newborn and fetal death.2 Such imperfections of shared mechanisms of immune tolerance between pregnancy and cancer suggest that cancer rejection via immunologic means may be possible, even considering the myriad mechanisms extending immunologic privilege to the fetus as well as cancer cells.This review summarizes the parallels in proliferation, invasion, and immune privilege between cancer and pregnanc...

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“…The first evidence for a role of IDO in immune regulation was observed when IDO expression was induced following viral infection or treatment with interferon (IFNγ), an important inflammatory cytokine (Yoshida et al, 1979;Yoshida et al, 1981). A prior observation that IDO is present in the urine of cancer patients then re-surfaced and its importance reevaluated (Rose, 1967).…”

Section: Ido In the Immune Systemmentioning

confidence: 99%

“…Another recent study has revealed that the cytotoxic agent β-lapachone is a direct inhibitor of IDO, postulating that this cytotoxic agent may benefit from the additional immunological effects that derive from its potent uncompetitive inhibitory effects on IDO1 activity. Other drugs in use include NSAIDs that indirectly block IDO activity as a result of COX2 inhibition (Sayama et al, 1981). Another effective IDO inhibitor in mouse studies is the anti-inflammatory ethyl pyruvate, which by inhibiting NF-kB activity blocks IDO expression and produces robust anti-tumor responses that are both T cell and IDO dependent (Muller et al, 2010).…”

Section: Clinical Trials Of Ido Inhibitorsmentioning

confidence: 99%

Inflammatory programming and immune modulation in cancer by IDO

Smith¹,

Prendergast²

2013

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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Immune dysregulation is one of the hallmarks of tumor growth and progression, a key event that allows for tumor evasion of the host immune system. More recent cancer modalities are embracing combinations incorporating immunotherapy with more traditional chemotherapy and radiotherapy. Traditional approaches are difficult to tolerate for the patient and become less effective as tumors evolve to survive these treatments. Immunotherapy has the benefit of reduced toxicity as it utilizes the patient's own immune system to identify and eliminate tumor cells. One mechanism manipulated by tumors is upregulation of the immunoregulatory enzyme indoleamine 2,3-dioxygenase (IDO). In this review, we focus on the mechanism by which tumors use IDO to evade detection by T cell immunity, as well as on novel small molecules that inhibit it as a cancer therapeutic strategy. Diversity of IDO-related immunoregulatory enzymes

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Inhibition of interferon-mediated induction of indoleamine 2,3-dioxygenase in mouse lung by inhibitors of prostaglandin biosynthesis.

Cited by 41 publications

References 26 publications

Role of indoleamine 2,3-dioxygenase in health and disease

Role of indoleamine 2,3-dioxygenase in health and disease

Cancer and Pregnancy: Parallels in Growth, Invasion, and Immune Modulation and Implications for Cancer Therapeutic Agents

Inflammatory programming and immune modulation in cancer by IDO

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