The new ‘5-HT’ hypothesis of depression: Cell-mediated immune activation induces indoleamine 2,3-dioxygenase, which leads to lower plasma tryptophan and an increased synthesis of detrimental tryptophan catabolites (TRYCATs), both of which contribute to the onset of depression

@article{Maes2011TheN,
  title={The new ‘5-HT’ hypothesis of depression: Cell-mediated immune activation induces indoleamine 2,3-dioxygenase, which leads to lower plasma tryptophan and an increased synthesis of detrimental tryptophan catabolites (TRYCATs), both of which contribute to the onset of depression},
  author={Michael Maes and Brian E. Leonard and Aye Mu Myint and Marta Kubera and Robert Verkerk},
  journal={Progress in Neuro-Psychopharmacology and Biological Psychiatry},
  year={2011},
  volume={35},
  pages={702-721}
}
Somatization, but not depression, is characterized by disorders in the tryptophan catabolite (TRYCAT) pathway, indicating increased indoleamine 2,3-dioxygenase and lowered kynurenine aminotransferase activity.
TLDR
Somatization is characterized by increased IDO activity and disorders in KAT activity and an increased neurotoxic potential, and the TRYCAT pathway may play a role in the pathophysiology of somatizing and "psychosomatic" symptoms.
Activation of Brain Indoleamine-2,3-dioxygenase Contributes to Depressive-Like Behavior Induced by an Intracerebroventricular Injection of Streptozotocin in Mice
TLDR
Evidence that IDO plays a critical role in mediating inflammation-induced depression is provided and the notion that neuroinflammation and the kynurenine pathway are important targets for novel therapeutic drugs for depression is supported.
Indoleamine-2,3-Dioxygenase/Kynurenine Pathway as a Potential Pharmacological Target to Treat Depression Associated with Diabetes
TLDR
The hypothesis that neuroinflammation in the HIP followed by IDO activation with a consequent decrease in the 5-HT levels can be a possible pathophysiological mechanism that links depression to diabetes is supported.
Indoleamine-2,3-dioxygenase-1 is a molecular target for the protective activity of mood stabilizers against mania-like behavior induced by d-amphetamine.
  • Hai-Quyen TranE. Shin Hyoung‐Chun Kim
  • Biology, Psychology
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • 2019
Plasma indoleamine-2,3-dioxygenase (IDO) is increased in drug-naïve major depressed patients and treatment with sertraline and ketoprofen normalizes IDO in association with pro-inflammatory and immune-regulatory cytokines.
TLDR
MDD is accompanied by activated immune-inflammatory pathways (including IDO) and the compensatory immune-regulatory system (CIRS), and the clinical efficacy of antidepressant treatment may be ascribed at least in part to decrements in IDO and the immune- inflammatory response.
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TLDR
It is concluded that kynurenine, kynurenic acid, and xanthurenic Acid have anti-inflammatory effects trough a reduction of IFNgamma, whereas quinolinic acid has pro- inflammatory effects in particular via significant decreases in IL-10.
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TLDR
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This paper hypothesizes that inflammatory, oxidative and nitrosative (IO&NS) pathways, and an increased translocation of LPS from gram-negative bacteria are causally related to depression following
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TLDR
Peripheral administration of IFN-α activated IDO in concert with central cytokine responses, resulting in increased brain KYN and QUIN, which correlated with depressive symptoms.
Interferon-γ and Tumor Necrosis Factor-α Mediate the Upregulation of Indoleamine 2,3-Dioxygenase and the Induction of Depressive-Like Behavior in Mice in Response to Bacillus Calmette-Guérin
TLDR
It is demonstrated that IFNγ, with TNFα, is necessary for induction of IDO and depressive-like behavior in mice after BCG infection and synergized to induce IDO in primary microglia.
Indoleamine 2,3-dioxygenase, an immunomodulatory protein, is suppressed by (-)-epigallocatechin-3-gallate via blocking of gamma-interferon-induced JAK-PKC-delta-STAT1 signaling in human oral cancer cells.
TLDR
EGCG, the major constituent of green tea, is found to significantly inhibit the expression of IDO in human oral cancer cell lines, indicating that EGCG is a potential drug for immune and target therapy to enhance cancer therapy by increasing antitumor immunity.
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