Evidence map›Paper›PMID 11507170›Full record

ArticleThe Journal of physiology2001

Tryptophan degradation by human placental indoleamine 2,3-dioxygenase regulates lymphocyte proliferation.

Y Kudo, C A Boyd, I L Sargent, C W Redman

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In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
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

26 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Human placental extract suppresses mast cell activation and induces mast cell apoptosis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Chromatographic analysis of tryptophan metabolites.Journal of separation science · 2017
    Review
  12. Kynurenic acid downregulates IL-17/1L-23 axis in vitro.Molecular and cellular biochemistry · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
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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

4 authors at 2 institutions in 1 country.

Y KudoDepartment of Human Anatomy and Genetics, University of Oxford, Oxford OX1 3QX, UK. yoshiki.kudo@anat.ox.ac.uk
C A Boyd
I L Sargent
C W Redman
John Radcliffe Hospital · GBUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The physiological importance of human placental indoleamine 2,3-dioxygenase (EC 1.13.11.42), the first and rate-limiting enzyme in tryptophan metabolism, in regulating feto-maternal immunology has been studied. 2. Concentrations were measured in placental villous explant conditioned media of 14 amino acids that are known to be required for lymphocyte proliferation. In the absence of interferon-gamma only tryptophan and threonine were significantly lowered; in the presence of interferon-gamma (known to stimulate indoleamine 2,3-dioxygenase) tryptophan but not threonine depletion was much greater. 3. Peripheral blood mononuclear cell proliferation determined by measuring thymidine incorporation into DNA following culture in the medium previously conditioned by culture of villous explants was markedly reduced when placental indoleamine 2,3-dioxygenase was stimulated with interferon-gamma. Inhibition of placental indoleamine 2,3-dioxygenase by 1-methyl-tryptophan prevented inhibition of thymidine incorporation. Supplementation of the conditioned medium with tryptophan but no other amino acid completely reversed the inhibition of thymidine incorporation. 4. Flow cytometric analysis showed that CD4-positive T lymphocyte division was specifically suppressed by indoleamine 2,3-dioxygenase-mediated tryptophan depletion. This inhibition of T cell proliferation was due to arrest of cell cycle progression. 5. To study the mechanism of tryptophan sensing we examined the ability of 11 L-tryptophan analogues to support lymphocyte proliferation. Only L-tryptophan methyl and ethyl esters were able to stimulate proliferation in tryptophan-free media. Since both of these molecules are readily degraded to tryptophan by intracellular esterases this suggests that the tryptophan sensor is intracellular. 6. Our results show that mechanisms are present in the human placenta which are able to regulate cellular proliferation of the maternal immune system. This mechanism is dependent both on placental indoleamine 2,3-dioxygenase-mediated tryptophan degradation and on tryptophan sensing systems within lymphocytes.

Indexed as

Amino AcidsCell DivisionChorionic VilliCulture MediaCulture Media, ConditionedFemaleFlow CytometryHumansIndoleamine-Pyrrole 2,3,-DioxygenaseLymphocytesMonocytesOsmolar ConcentrationPhytohemagglutininsPlacentaPregnancyTime FactorsAmino AcidsCulture MediaCulture Media, ConditionedIndoleamine-Pyrrole 2,3,-DioxygenasePhytohemagglutininsTryptophanTryptophan Oxygenase

Identifiers

PMID11507170
PMCPMC2288791
OpenAlexW2002775741

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.