Evidence map›Paper›PMID 24391212›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

The SOCS3-independent expression of IDO2 supports the homeostatic generation of T regulatory cells by human dendritic cells.

Sara Trabanelli, Darina Očadlíková, Marilena Ciciarello, Valentina Salvestrini, Mariangela Lecciso, Camilla Jandus, Richard Metz, Cecilia Evangelisti, Lisa Laury-Kleintop, Pedro Romero and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Review
  3. Investigation of the Impact of Tryptophan-Metabolizing Enzymes and Kynurenic Acid on Antibody-Mediated Glomerulonephritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Immune cell engineering: opportunities in lung cancer therapeutics.Drug delivery and translational research · 2020
    Review
  19. Article
  20. Review
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

13 authors at 6 institutions in 3 countries.

Sara TrabanelliDepartment of Specialistic, Diagnostic, and Experimental Medicine, Institute of Hematology "Seràgnoli," University of Bologna, 40138 Bologna, Italy;
Darina Očadlíková
Marilena Ciciarello
Valentina Salvestrini
Mariangela Lecciso
Camilla Jandus
Richard Metz
Cecilia Evangelisti
Lisa Laury-Kleintop
Pedro Romero
George C Prendergast
Antonio Curti
Roberto M Lemoli
University of Bologna · ITIstituto Oncologico Romagnolo · ITLankenau Institute for Medical Research · USLudwig Cancer Research · CHNewLink Genetics (United States) · USUniversity of Lausanne · CH

Funding

IDO Inhibitors for Combinatorial Cancer TherapyR01CA109542 · NCI · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI PRENDERGAST, GEORGE C · 2005 to 2015
$2.0M
IDO2 Targeting for pancreatic cancer treatmentR21CA159337 · NCI · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI PRENDERGAST, GEORGE C · 2011 to 2012
$401k
NCI NIH HHS CA109542NCI NIH HHS CA159337NCI NIH HHS R01 CA109542NCI NIH HHS R21 CA159337
6 · The paper itself

Abstract

Dendritic cells (DCs) are professional APCs that have a role in the initiation of adaptive immune responses and tolerance. Among the tolerogenic mechanisms, the expression of the enzyme IDO1 represents an effective tool to generate T regulatory cells. In humans, different DC subsets express IDO1, but less is known about the IDO1-related enzyme IDO2. In this study, we found a different pattern of expression and regulation between IDO1 and IDO2 in human circulating DCs. At the protein level, IDO1 is expressed only in circulating myeloid DCs (mDCs) and is modulated by PGE2, whereas IDO2 is expressed in both mDCs and plasmacytoid DCs and is not modulated by PGE2. In healthy subjects, IDO1 expression requires the presence of PGE2 and needs continuous transcription and translation, whereas IDO2 expression is constitutive, independent from suppressor of cytokine signaling 3 activity. Conversely, in patients suffering from inflammatory arthritis, circulating DCs express both IDO1 and IDO2. At the functional level, both mDCs and plasmacytoid DCs generate T regulatory cells through an IDO1/IDO2-dependent mechanism. We conclude that, in humans, whereas IDO1 provides an additional mechanism of tolerance induced by proinflammatory mediators, IDO2 is stably expressed in steady-state conditions and may contribute to the homeostatic tolerogenic capacity of DCs.

Indexed as

Arthritis, PsoriaticArthritis, RheumatoidCells, CulturedDendritic CellsDinoprostoneEnzyme InductionHomeostasisHumansImmune ToleranceIndoleamine-Pyrrole 2,3,-DioxygenaseMonocytesOrgan SpecificityProtein BiosynthesisRNA InterferenceRNA, Small InterferingSpondylitis, AnkylosingDinoprostoneIDO1 protein, humanIDO2 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseRNA, Small InterferingSOCS3 protein, humanSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTryptophan

Identifiers

PMID24391212
PMCPMC3905741
OpenAlexW1489511844

What OpenQuestion holds

Textmetadata
LicenceTDM
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.