Indoleamine-Pyrrole 2,3,-Dioxygenase (Indoleamine 2,3 Dioxygenase)

A dioxygenase with specificity for the oxidation of the indoleamine ring of TRYPTOPHAN. It is an extrahepatic enzyme that plays a role in metabolism as the first and rate limiting enzyme in the kynurenine pathway of TRYPTOPHAN catabolism.
Also Known As:
Indoleamine 2,3 Dioxygenase; IDO Dioxygenase; Indolamine-2,3-Dioxygenase; Indoleamine 2,3-Dioxygenase; Indoleamine-Oxygen 2,3-Oxidoreductase (Decyclizing); Dioxygenase, IDO; Indolamine 2,3 Dioxygenase
Networked: 549 relevant articles (7 outcomes, 34 trials/studies)

Relationship Network

Bio-Agent Context: Research Results


1. Mellor, Andrew L: 21 articles (10/2014 - 04/2002)
2. Takikawa, Osamu: 21 articles (08/2014 - 01/2003)
3. Munn, David H: 19 articles (10/2015 - 04/2002)
4. Prendergast, George C: 15 articles (07/2014 - 03/2005)
5. Saito, Kuniaki: 14 articles (09/2015 - 02/2008)
6. Fuchs, Dietmar: 14 articles (05/2015 - 10/2004)
7. Muller, Alexander J: 14 articles (07/2014 - 03/2005)
8. Sakurai, Kenichi: 11 articles (10/2015 - 08/2002)
9. Puccetti, Paolo: 11 articles (01/2015 - 03/2005)
10. Enomoto, Katsuhisa: 10 articles (10/2015 - 10/2004)

Related Diseases

1. Hypersensitivity (Allergy)
06/01/2012 - "The indoleamine 2,3-dioxygenase (IDO) pathway controls allergy."
01/01/2009 - "Indoleamine 2,3-dioxygenase (IDO) in inflammation and allergy to Aspergillus."
04/15/2002 - "Pharmacological inhibition of indoleamine 2,3-dioxygenase (IDO) activity during murine gestation results in fetal allograft rejection and blocks the ability of murine CD8(+) dendritic cells to suppress delayed-type hypersensitivity responses to tumor-associated peptide Ags. "
09/01/2007 - "Recent results have shown that Talpha1: (a) primed DCs for antifungal Th1 resistance through Toll-like receptor (TLR)/MyD88-dependent signaling and this translated in vivo in protection against aspergillosis; (b) activated plasmacytoid DCs (pDC) via the TLR9/MyD88-dependent viral recognition, thus leading to the activation of interferon regulatory factor 7 and the promotion of the IFN-alpha/IFN-gamma-dependent effector pathway, which resulted in vivo in protection against primary murine cytomegalovirus infection; (c) induced indoleamine 2,3-dioxygenase activity in DCs, thus affecting tolerization toward self as well as microbial non-self-antigens, and this resulted in vivo in transplantation tolerance and protection from inflammatory allergy. "
01/01/2015 - "Diphencyprone (DPCP) is a hapten that causes delayed-type hypersensitivity (DTH) reactions in human skin, and is used as a topical therapeutic for alopecia areata, warts, and cutaneous melanoma metastases.  We examined peak DTH reactions induced by DPCP (3 days post-challenge) by comprehensive gene expression and histological analysis.  To better understand how these DTH reactions naturally resolve, we compared our DPCP biopsies to those from patients with psoriasis vulgaris, a chronic inflammatory disease that does not resolve.  By both microarray and qRT-PCR, we found that psoriasis lesional skin has significantly lower expression of many negative immune regulators compared to peak DPCP reactions.  These regulators include: interleukin-10, cytotoxic T lymphocyte-associated 4 (CTLA4), programmed cell death 1 (PD1), programmed cell death 1 ligand 1 (PDL1), programmed cell death 1 ligand 2 (PDL2), and indoleamine 2,3-dioxygenase (IDO1).  Their decreased expression was confirmed at the protein level by immunohistochemistry.  To more completely determine the balance of positive vs. negative immune regulators in both DPCP reactions and psoriasis, we developed one comprehensive gene list for positive regulatory (inflammatory) genes, and another for negative regulatory (immunosuppressive) genes, through Gene Ontology terms and literature review.  With this approach, we found that DPCP reactions have a higher ratio of negative to positive regulatory genes (both in terms of quantity and expression levels) than psoriasis lesional skin.  These data suggest that the disease chronicity that distinguishes psoriasis from transient DTH reactions may be related to absence of negative immune regulatory pathways, and induction of these is therefore of therapeutic interest.  Further study of these negative regulatory mechanisms that are present in DPCP reactions, but not in psoriasis, could reveal novel players in the pathogenesis of chronic inflammation.  The DPCP system used here thus provides a tractable model for primary discovery of pathways potentially involved in immune regulation in peripheral tissues. "
2. Neoplasms (Cancer)
3. Inflammation
4. Infection
5. Melanoma (Melanoma, Malignant)

Related Drugs and Biologics

1. Tryptophan (L-Tryptophan)
2. Interleukin-10 (Interleukin 10)
3. diphenylcyclopropenone
4. Toll-Like Receptors (Toll-Like Receptor)
5. Small Interfering RNA (siRNA)
6. Interferon Regulatory Factor-7 (Interferon Regulatory Factor 7)
7. Estrogens (Estrogen)
8. Autoantigens
9. Kynurenine
10. Arginase

Related Therapies and Procedures

1. Homologous Transplantation (Allograft)
2. Transplants (Transplant)
3. Drug Therapy (Chemotherapy)
4. Transplantation (Transplant Recipients)
5. Hematopoietic Stem Cell Transplantation