Evidence map›Paper›PMID 34202246›Full record

ReviewBiomedicines2021

Immune Influencers in Action: Metabolites and Enzymes of the Tryptophan-Kynurenine Metabolic Pathway.

Masaru Tanaka, Fanni Tóth, Helga Polyák, Ágnes Szabó, Yvette Mándi, László Vécsei

Abstract readReview
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

161 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  7. Altered Kynurenine Pathway Metabolism in Drug-naive Children and Adolescents with Generalized Anxiety Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
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101 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Masaru TanakaMTA-SZTE-Neuroscience Research Group, H-6725 Szeged, Hungary.ORCID 0000-0003-4383-4024
Fanni TóthMTA-SZTE-Neuroscience Research Group, H-6725 Szeged, Hungary.
Helga PolyákInterdisciplinary Excellence Centre, Department of Neurology, Faculty of Medicine, University of Szeged, H-6725 Szeged, Hungary.
Ágnes SzabóInterdisciplinary Excellence Centre, Department of Neurology, Faculty of Medicine, University of Szeged, H-6725 Szeged, Hungary.
Yvette MándiDepartment of Medical Microbiology and Immunology, Faculty of Medicine, University of Szeged, H-6720 Szeged, Hungary.
László VécseiMTA-SZTE-Neuroscience Research Group, H-6725 Szeged, Hungary.

Funding

EFOP 3.6.3-VEKOP-16-2017-00009GINOP 2.3.2-15-2016-00034GINOP 2.3.2-15-2016-00048New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund ÚNKP-20-3TKP2020 Thematic Excellence Programme 2020University of Szeged Open Access Fund 4942
6 · The paper itself

Abstract

The tryptophan (TRP)-kynurenine (KYN) metabolic pathway is a main player of TRP metabolism through which more than 95% of TRP is catabolized. The pathway is activated by acute and chronic immune responses leading to a wide range of illnesses including cancer, immune diseases, neurodegenerative diseases and psychiatric disorders. The presence of positive feedback loops facilitates amplifying the immune responses vice versa. The TRP-KYN pathway synthesizes multifarious metabolites including oxidants, antioxidants, neurotoxins, neuroprotectants and immunomodulators. The immunomodulators are known to facilitate the immune system towards a tolerogenic state, resulting in chronic low-grade inflammation (LGI) that is commonly present in obesity, poor nutrition, exposer to chemicals or allergens, prodromal stage of various illnesses and chronic diseases. KYN, kynurenic acid, xanthurenic acid and cinnabarinic acid are aryl hydrocarbon receptor ligands that serve as immunomodulators. Furthermore, TRP-KYN pathway enzymes are known to be activated by the stress hormone cortisol and inflammatory cytokines, and genotypic variants were observed to contribute to inflammation and thus various diseases. The tryptophan 2,3-dioxygenase, the indoleamine 2,3-dioxygenases and the kynurenine-3-monooxygenase are main enzymes in the pathway. This review article discusses the TRP-KYN pathway with special emphasis on its interaction with the immune system and the tolerogenic shift towards chronic LGI and overviews the major symptoms, pro- and anti-inflammatory cytokines and toxic and protective KYNs to explore the linkage between chronic LGI, KYNs, and major psychiatric disorders, including depressive disorder, bipolar disorder, substance use disorder, post-traumatic stress disorder, schizophrenia and autism spectrum disorder.

Indexed as

autism spectrum disorderbipolar disorderchronic inflammationdepressionimmune toleranceinflammatory factorkynurenic acidkynureninelow-grade inflammationpost-traumatic stress disorderschizophreniasubstance use disorder

Identifiers

PMID34202246
PMCPMC8301407

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.