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Human Polyclonal IDO1 Primary Antibody für ICC, FACS - ABIN1169196
Boasso, Herbeuval, Hardy, Anderson, Dolan, Fuchs, Shearer: HIV inhibits CD4+ T-cell proliferation by inducing indoleamine 2,3-dioxygenase in plasmacytoid dendritic cells. in Blood 2007
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Mouse (Murine) Polyclonal IDO1 Primary Antibody für ICC, IHC - ABIN1169195
Yadav, Burudi, Alirezaei, Flynn, Watry, Lanigan, Fox: IFN-gamma-induced IDO and WRS expression in microglia is differentially regulated by IL-4. in Glia 2007
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Human Polyclonal IDO1 Primary Antibody für ELISA, WB - ABIN543533
Scheler, Wenzel, Tüting, Takikawa, Bieber, von Bubnoff: Indoleamine 2,3-dioxygenase (IDO): the antagonist of type I interferon-driven skin inflammation? in The American journal of pathology 2007
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Human Monoclonal IDO1 Primary Antibody für FACS - ABIN4896118
Lood, Tydén, Gullstrand, Klint, Wenglén, Nielsen, Heegaard, Jönsen, Kahn, Bengtsson: Type I interferon-mediated skewing of the serotonin synthesis is associated with severe disease in systemic lupus erythematosus. in PLoS ONE 2015
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Human Monoclonal IDO1 Primary Antibody für FACS - ABIN4896116
Kaltenmeier, Gawanbacht, Beyer, Lindner, Trzaska, van der Merwe, Härter, Grüner, Fabricius, Lotfi, Schwarz, Schütz, Hönig, Schulz, Kern, Bommer, Schrezenmeier, Kirchhoff, Jahrsdörfer: CD4+ T cell-derived IL-21 and deprivation of CD40 signaling favor the in vivo development of granzyme B-expressing regulatory B cells in HIV patients. in Journal of immunology (Baltimore, Md. : 1950) 2015
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Human Polyclonal IDO1 Primary Antibody für IF (cc), IF (p) - ABIN1714836
Fu, Zhang, Song, Sheng, Li, Li, Song, Wang, Chu, Wei: Effect of bone marrow-derived CD11b(+)F4/80 (+) immature dendritic cells on the balance between pro-inflammatory and anti-inflammatory cytokines in DBA/1 mice with collagen-induced arthritis. in Inflammation research : official journal of the European Histamine Research Society ... [et al.] 2014
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Mouse (Murine) Polyclonal IDO1 Primary Antibody für WB - ABIN549032
Suzuki, Toné, Takikawa, Kubo, Kohno, Minatogawa: Expression of indoleamine 2,3-dioxygenase and tryptophan 2,3-dioxygenase in early concepti. in The Biochemical journal 2001
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Human Monoclonal IDO1 Primary Antibody für FACS - ABIN4896114
Chimal-Ramírez, Espinoza-Sánchez, Chávez-Sánchez, Arriaga-Pizano, Fuentes-Pananá: Monocyte Differentiation towards Protumor Activity Does Not Correlate with M1 or M2 Phenotypes. in Journal of immunology research 2016
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Mouse (Murine) Monoclonal IDO1 Primary Antibody für FACS, IP - ABIN1043733
Mellor, Munn: IDO expression by dendritic cells: tolerance and tryptophan catabolism. in Nature reviews. Immunology 2004
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.
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 role of IDO1-IDO2-AHR pathway in the TLR4-induced tolerogenic phenotype in human dendritic cells has been reported.
High coexpression of cytoplasmic IDO1/COX2 was found to be an independent predictor of poor outcome in colorectal cancer patients.
Report the crystal structures of IDO1 in complex with its substrate, Trp, an inhibitor, epacadostat, and/or an effector, indole ethanol (IDE). The data reveal structural features of the active site (Sa) critical for substrate activation; in addition, they disclose a new inhibitor-binding mode and a distinct small molecule binding site (Si).
IDO decreased glycolysis and glutaminolysis by activating GCN2K, resulting in activation of AMPactivated protein kinase.
this review highlights the role of indoleamine-2,3-dioxygenase in normal and pathological pregnancies
Data suggest that IDO1 is constitutively expressed in insulin-secreting cells from donors without diabetes; IDO1 appears to be down-regulated in insulin-containing beta-cells from double autoantibody-positive donors and donors with recent-onset type 1 diabetes; this study was conducted on donor tissues obtained from cadavers.
Twenty-nine percent (n = 2/7) of the PD-L1 positive poorly differentiated thyroid carcinomas also co-expressed IDO1
In non-ST segment elevation myocardial infarction, the tolerogenic mechanism of the immune response related to IDO production by activated monocytes derived dendritic cells is altered, supporting their role in T-cell dysregulation.
These data suggest that the expression of immunosuppressive molecules, including PD-1 ligands and IDO1, by macrophage/microglia may be involved in immune evasion of lymphoma cells.
Our data demonstrate that high intratumoral IDO1 mRNA levels correlate with a poor glioblastoma (GBM) patient prognosis. It also confirms the positive correlation between increased GBM IDO1 levels and human-infiltrating T cells
Among the 89 patients, CD274, LAG3, and IDO1 expressions in TIICs were observed in 68.6% (61 cases), 13.5% (12), and 28.1% (25) of patients, respectively. CD274, CTLA4, and IDO1 were expressed in tumor cells of 24.7% (22 cases), 4.5% (4), and 72.0% (64) of patients, respectively.
Multivariate analysis indicated indoleamine 2,3-dioxygenase (IDO) expression as independent prognostic factors in overall survival (OS).
these findings suggest that IDO1 promoter methylation regulates anti-immune responses in breast cancer subtypes and could be used as a predictive biomarker for IDO1 inhibitor-based immunotherapy.
main biological and actionable difference between OSCC from NSND and SD lies in the immune microenvironment, suggesting a higher clinical benefit of PD-L1 and IDO1 inhibition in OSCC from NSND
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.
Aortic Plasmacytoid dendritic cells expressed CCR9 and indoleamine 2,3-dioxygenase 1 (IDO-1), an enzyme involved in driving the generation of regulatory T cells (Tregs).
Indoleamine-2,3-dioxygenase (IDO) production by Plasmacytoid dendritic cells (pDCs)is necessary to confer suppressive function to T-Cells, Regulatory (Tregs) in experimental autoimmune encephalomyelitis (EAE).
our findings support the hypothesis elevated IDO activity in non-CNS due to virus infections causes pain hypersensitivity
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