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Differential expression of CD25 and IDO mRNA with high and low virulence bovine viral diarrhea virus might reflect temporal differences in transcription during the immune response elicited by these viral strains.
IDO may be involved in downregulating immune responses to M. avium subsp. paratuberculosis and other virulent mycobacteria, which may be an example of the pathogen harnessing host immunoregulatory pathways to aid survival.
INDO participates in IFN-gama-induced death of bovine luteal cells, through a mechanism that involves degradation of tryptophan, thereby reducing tryptophan concentrations to a point insufficient to meet luteal cells needs
SIV-infected macaques exhibiting progression to AIDS displayed greater expression of TGF-beta and indoleamine 2,3 dioxygenase in CD8+ T cells from mesentric lymph nodes.
IDO-1 is commonly expressed by non-small cell lung cancers... its frequent coexpression with PD-L1 may account for the increased efficacy seen with dual blockade of PD-1/PD-L1 and IDO in clinical studies.
A urine-based mRNA biomarker study revealed the diagnostic potential of IDO gene expression in urine of men at risk of prostate cancer development.
Indoleamine 2, 3-dioxygenase 1 (IDO1) expression levels correlated inversely with IDO1 promoter methylation levels.
The aim of the study was to develop a practical and objective immunohistochemical technique to quantify IDO-1 expression on diagnostic bone marrow biopsies of acute myeloid leukemia patients.
IDO activity, expressed as kynurenine/tryptophan ratio, is associated with response to immunotherapy.
DNA methylation analysis in humans shows that IDO1 is hypermethylated in human sperm but partially methylated in placentas, suggesting similar methylation patterns to mouse.
We conclude that an active hCMV infection in the eye might favor the replication of pathogens causing co-infections in immunosuppressed individuals. An hCMV caused blockade of IDO1 might weaken the eye's immune privilege and favor the development of post-infectious autoimmune uveitis.
Expression of PD-L1 and IDO is seen in a subset of high-grade serous ovarian carcinoma from African American women and is correlated with elevated lymphocyte infiltration.
Human indoleamine 2,3-dioxygenase 1 (hIDO1) and tryptophan dioxygenase (hTDO) catalyze the same dioxygenation reaction of Trp to generate N-formyl kynurenine (NFK). They share high structural similarity, especially in the active site. However, hIDO1 possesses a unique inhibitory substrate binding site (Si) that is absent in hTDO.
Results suggest that indoleamine 23-dioxygenase 1 (IDO1) and programmed cell death-ligand 1 (PD-L1) co-expression may define an aggressive form of lung adenocarcinoma.
human cardiac/stem progenitor cells exert an immune-suppressive effect on T lymphocyte proliferation through a paracrine mechanism associated with indoleamine 2,3-dioxygenase (IDO) enzyme-mediated tryptophan metabolism.
In summary, IDO and PD-L1 co-expression is common in cervical squamous cell carcinomas and, to a lesser extent, vulvar squamous cell carcinomas.
It is a immune checkpoint molecule and modulated during oral epithelial dysplastic changes, and their expression is associated with inflammatory cell infiltration in the lamina propria.
IDO induction within melanoma cells may directly reflect tumor progression.
In this work, we assessed the relationship between single-nucleotide polymorphisms (SNPs) of KAT1, KAT2 and IDO1 gene encoding, and the risk of depression development. Our study was performed on the DNA isolated from peripheral blood of 281 depressed patients and 236 controls. We genotyped, by using TaqMan probes, four polymorphisms.
IDO1 crystal structure with its substrate tryptophan.
Study revealed that IDO1 expression, which is common in hepatocellular carcinoma, is a positive survival predictor, and its expression is a counter-regulatory action to suppress the antitumor immune response.
High IDO1 expression is associated with cervical cancer.
Interference SNHG1 could inhibit the differentiation of Treg cells by promoting miR-448 expression and reducing IDO level, thereby impeding the immune escape of breast cancer .
We discuss how small-molecule inhibitors of the tryptophan (Trp) catabolic enzyme indoleamine 2,3-dioxygenase (IDO) represent a vanguard of new immunometabolic adjuvants to safely enhance the efficacy of cancer immunotherapy, radiotherapy, or 'immunogenic' chemotherapy by leveraging responses to tumor neoantigens
The current study shows that the Ido1 and Ido2 genes are imprinted and maternally expressed in mouse placentas. DNA methylation analysis demonstrates that nine CpG sites at the Ido1 promoter constitute a differentially methylated region that is highly methylated in sperm but unmethylated in oocytes
an unexpected function of indoleamine 2,3-dioxygenase in the fine tuning of intestinal tryptophan metabolism with major consequences on microbiota-dependent control of metabolic disease, is identified.
Data show that indoleamine 2,3 dioxygenase-1 (IDO1)/ miR-18a/ killer cell lectin-like receptor subfamily K (NKG2D/NKG2DL) regulatory axis in the regulation of NK cell function.
High IDO1 expression is associated with Poststroke Depression.
Influenza infection of NIH-3T3 cells elevates the expression of indoleamine 2,3 dioxygenase (IDO). Inhibition against IDO followed by infection increases the level of viral RNA and reduces the upregulation of 3-hydroxyanthranilate 3,4-dioxygenase driven by virus. Induction of IDO appears to contribute to limiting replication of the WSN/33 strain of influenza A virus in murine NIH-3T3 cells.
The treatment of Salmonella enterica serovar choleraesuis or resveratrol in murine melanoma cells demonstrated the ability of reducing IDO1 production through upregulating Cx43.
Study showed that the knockout of IDO prevented vascular smooth muscle cells apoptosis in AngII -treated Ldlr-/- mice fed with HFD, suggesting a detrimental role of IDO in abdominal aortic aneurysm formation.
The KYNurenine pathway of IDO1-mediated Tryptophan metabolism plays a critical role in depressive symptoms associated with IFN-alpha therapy.
IDO is a critical regulator of acute pulmonary inflammation .
Data suggest that Indoleamine 2,3-dioxygenase 1 (IDO1) appears to be a potential hallmark of liver lesions, and its deficiency protects mice from CCl4-induced fibrosis mediated by Th17 cells down-regulation and tryptophan 2,3-dioxygenase (TDO) compensatory increase.
Indoleamine 2,3-dioxygenase regulates anti-tumor immunity in lung cancer by metabolic reprogramming of immune cells in the tumor microenvironment
Findings suggest non-redundant neurophysiological roles for indoleamine 2,3-dioxygenase 1, indoleamine 2,3-dioxygenase 2 and tryptophan 2,3-dioxygenase in modulating brain activities and metabolism.
These results show IDO is upregulated with RSV infection and this upregulation likely participates with IFN-gamma in inhibition of virus replication and suppression of some host cell responses to infection.
Lipopolysaccharide (LPS) stimulation increased the expression and activity of the immunoregulatory enzyme IDO1 in hepatic stellate cells (HSCs), and LPS/HSCs stimulated aryl hydrocarbon receptor (AhR) signaling in cocultured regulatory T cells.
this study shows that the presence of IFN-alpha at antigen sensitization activates an IDO1/TGF-beta-dependent anti-inflammatory program that upon antigenic rechallenge prevents inflammation via plasmacytoid dendritic cells
The deficiency of indoleamine 2,3-dioxygenase aggravates the carbon tetrachloride-induced liver fibrosis in mice.
Across strains, networks depicted a predominance of genes under-expressed in microglia relative to macrophages that may be a precursor for the different response of both cell types to challenges. The detected transcriptome differences enhance the understanding of the role of IDO1 in the microglia transcriptome under unchallenged conditions.
Data show that indoleamine 23-dioxygenase 1 (IDO-1) inhibitors 1-methyl-D-tryptophan was able to alleviate most of the behavioural changes resulting from unpredictable chronic mild stress (UCMS) exposure.
IDO did not play a pivotal role in the suppression of allergic airway inflammation through adipose-derived stem cells, suggesting that it is not the major regulator responsible for suppressing allergic airway inflammation.
These results indicate that Platelet-activating Factor -mediated endotoxin tolerance is initiated via IDO- and JAK/STAT-dependent expression of SOCS3.
elevated activity and protein expression levels following lipopolysaccharide stimulation
This gene encodes indoleamine 2,3-dioxygenase (IDO) - a heme enzyme that catalyzes the first and rate-limiting step in tryptophan catabolism to N-formyl-kynurenine. This enzyme acts on multiple tryptophan substrates including D-tryptophan, L-tryptophan, 5-hydroxy-tryptophan, tryptamine, and serotonin. This enzyme is thought to play a role in a variety of pathophysiological processes such as antimicrobial and antitumor defense, neuropathology, immunoregulation, and antioxidant activity. Through its expression in dendritic cells, monocytes, and macrophages this enzyme modulates T-cell behavior by its peri-cellular catabolization of the essential amino acid tryptophan.
indoleamine-pyrrole 2,3 dioxygenase
, indoleamine 2,3-dioxygenase 2
, putative indoleamine 2,3-dioxygenase
, indoleamine 2,3-dioxygenase 1
, indolamine 2,3 dioxygenase
, indole 2,3-dioxygenase
, indoleamine-pyrrole 2,3-dioxygenase
, indoleamine 23-dioxygenase