The importance of cytokines and autoantibodies in depression.
Campinas, Brazil. In Autoimmun Rev, 18 Oct 2014
Tumor necrosis factor alpha (TNF-α) may underlie the mechanism of depression by an activation of the hypothalamo-pituitary-adrenocortical (HPA) axis, an activation of neuronal serotonin transporters and the stimulation of the indoleamine 2,3-dioxygenase which leads to tryptophan depletion.
The tryptophan utilization concept in pregnancy.
Cardiff, United Kingdom. In Obstet Gynecol Sci, Jul 2014
The decrease in maternal plasma total (free + albumin-bound) tryptophan (Trp) during the third pregnancy trimester is attributed to induction of indoleamine 2,3-dioxygenase (IDO).
Antioxidants, inflammation and cardiovascular disease.
Graz, Austria. In World J Cardiol, Jul 2014
During cellular immune response, interferon γ-dependent pathways are activated such as tryptophan breakdown by the enzyme indoleamine 2,3-dioxygenase (IDO) in monocyte-derived macrophages, fibroblasts, endothelial and epithelial cells.
Neuroinflammation and comorbidity of pain and depression.
Houston, United States. In Pharmacol Rev, Dec 2013
These mechanisms include direct effects of cytokines on the neuronal environment or indirect effects via downregulation of G protein-coupled receptor kinase 2, activation of the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase that generates neurotropic kynurenine metabolites, increased brain extracellular glutamate, and the switch of GABAergic neurotransmission from inhibition to excitation.
The role of placental tryptophan catabolism.
Graz, Austria. In Front Immunol, Dec 2013
This review discusses the mechanisms and consequences of degradation of tryptophan (Trp) in the placenta, focusing mainly on the role of indoleamine 2,3-dioxygenase-1 (IDO1), one of three enzymes catalyzing the first step of the kynurenine pathway of Trp degradation.
Highlights of 10 years of immunology in Nature Reviews Immunology.
New Haven, United States. In Nat Rev Immunol, 2011
Highlights include our improved understanding of Toll-like receptor signalling, and of immune regulation mediated by regulatory T cells, indoleamine 2,3-dioxygenase, myeloid-derived suppressor cells and interleukin-10.