Tumor immune escape mediated by indoleamine 2,3-dioxygenase

Ζαμανάκου, Μαρία; Germenis, Anastasios E.; Karanikas, Vaios

doi:10.1016/j.imlet.2007.06.001

Cited by 105 publications

(99 citation statements)

References 76 publications

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“…Certain metabolites of the kynurenine pathway have also been shown to be immunosuppressive. [33][34][35][36] IDO affects dendritic cell function with a mean inhibition of 27.1% (SD 15.8%; p < 0.001, Wilcoxon test), whereas D-1MT failed to inhibit IDO activity with a mean inhibition of 2.2% (SD 7.7%; p = 0.10). This pattern of inhibition using these selective stereoisomers confirmed that cultured meningioma cells primarily express the IDO1 isoform to convert tryptophan via the kynurenine pathway.…”

Section: Resultsmentioning

confidence: 95%

In vivo metabolism of tryptophan in meningiomas is mediated by indoleamine 2,3-dioxygenase 1

Zitron¹,

Kamson²,

Kiousis³

et al. 2013

Cancer Biology & Therapy

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Section: Resultsmentioning

confidence: 95%

In vivo metabolism of tryptophan in meningiomas is mediated by indoleamine 2,3-dioxygenase 1

Zitron¹,

Kamson²,

Kiousis³

et al. 2013

Cancer Biology & Therapy

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“…Recent studies suggest IDO as a target for cancer suppression in vivo Mellor, 2004, 2007;Muller et al, 2005;Zamanakou et al, 2007). It has been shown previously that IDO inhibition induces a robust allogenic T-cell response in vitro and delays tumor growth in vivo (Friberg et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Characterization of the Kynurenine Pathway in Human Neurons

et al. 2007

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The kynurenine pathway is a major route of L-tryptophan catabolism producing neuroactive metabolites implicated in neurodegeneration and immune tolerance. We characterized the kynurenine pathway in human neurons and the human SK-N-SH neuroblastoma cell line and found that the kynurenine pathway enzymes were variably expressed. Picolinic carboxylase was expressed only in primary and some adult neurons but not in SK-N-SH cells. Because of this difference, SK-N-SH cells were able to produce the excitotoxin quinolinic acid, whereas human neurons produced the neuroprotectant picolinic acid. The net result of kynurenine pathway induction in human neurons is therefore predicted to result in neuroprotection, immune regulation, and tumor inhibition, whereas in SK-N-SH cells, it may result in neurotoxicity, immune tolerance, and tumor promotion. This study represents the first comprehensive characterization of the kynurenine pathway in neurons and the first description of the involvement of the kynurenine pathway as a mechanism for controlling both tumor cell neurotoxicity and persistence.

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“…2 Initial work of Musajo and Benassi 3 demonstrating increased urinary excretion of tryptophan metabolites of the kynurenine pathway in cancer patients followed by seminal work of Yasui et al 4 showing interferon γ (IFNγ)-mediated induction of IDO in lung cancer, paved the way for the more recent identification of increased expression of IDO by tumor cells 5 as well as for the attempts to clarify its possible role in tumor immune escape. 6 Mounting evidence indicates that, within the tumor microenvironment, not only tumor cells but also some subsets of tumor infiltrating cells, such as lymphocytes, dendritic cells and monocytes, can be sources of IDO. To this end, it is noteworthy to underline that, in a recent study, 7 IDO-producing tumor infiltrating eosinophils relate negatively with disease progression in non-small cell lung cancers (NSCLC).…”

Section: Introductionmentioning

confidence: 99%