Evidence map›Paper›PMID 27166946›Full record

ArticleCell metabolism2016

Indoleamine 2,3-Dioxygenase-Expressing Aortic Plasmacytoid Dendritic Cells Protect against Atherosclerosis by Induction of Regulatory T Cells.

Tae Jin Yun, Jun Seong Lee, Kawthar Machmach, Dahee Shim, Junhee Choi, Young Jin Wi, Hyung Seok Jang, In-Hyuk Jung, Kyeongdae Kim, Won Kee Yoon and 19 more

Erratum issuedOpen access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Cell metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  9. Complex Interplay Between Metabolism and CD4Cardiovascular drugs and therapy · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

29 authors at 13 institutions in 4 countries.

Tae Jin YunLaboratory of Cellular Physiology and Immunology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada; Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, QC H3A 1A3, Canada.
Jun Seong LeeLaboratory of Cellular Physiology and Immunology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada; Department of Microbiology, Infectiology, and Immunology, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Kawthar MachmachLaboratory of Cellular Physiology and Immunology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada; Department of Microbiology, Infectiology, and Immunology, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Dahee ShimDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul 133-791, South Korea.
Junhee ChoiDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul 133-791, South Korea.
Young Jin WiDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul 133-791, South Korea.
Hyung Seok JangDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul 133-791, South Korea.
In-Hyuk JungDepartment of Life Sciences, Ewha Womans University, Seoul 120-750, South Korea.
Kyeongdae KimDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul 133-791, South Korea.
Won Kee YoonLaboratory Animal Resource Center, KRIBB, Chungbuk 363-883, South Korea.
Mohammad Alam MiahLaboratory of Cellular Physiology and Immunology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada; Department of Microbiology, Infectiology, and Immunology, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Bin LiLaboratory of Cellular Physiology and Immunology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada; Department of Molecular Biology, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Jinsam ChangLaboratory of Cellular Physiology and Immunology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada; Department of Molecular Biology, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Mariana G BegoLaboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada.
Tram N Q PhamLaboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada.
Jakob LoschkoInstitute for Immunology, Ludwig-Maximilians-Universität München, München 80336, Germany.
Jörg Hermann FritzDepartment of Microbiology and Immunology, McGill University, Montréal, QC H3A 2B4, Canada.
Anne B KrugInstitute for Immunology, Ludwig-Maximilians-Universität München, München 80336, Germany.
Seung-Pyo LeeCardiovascular Center, and Department of Internal Medicine, Seoul National University Hospital, Seoul 110-744, South Korea.
Tibor KelerCelldex Therapeutics, Hampton, NJ 08827, USA.
Jean V GuimondCentre de Santé et de Services Sociaux Jeanne-Mance, Montréal, QC H2H 2B4, Canada.
Elie HaddadDepartment of Microbiology, Infectiology, and Immunology, Université de Montréal, Montréal, QC H3C 3J7, Canada; CHU Sainte-Justine Research Center, Montréal, QC H3T 1C5, Canada.
Eric A CohenDepartment of Microbiology, Infectiology, and Immunology, Université de Montréal, Montréal, QC H3C 3J7, Canada; Laboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada.
Martin G SiroisResearch Center, Montréal Heart Institute, Montréal, QC H1T 1C8, Canada; Department of Pharmacology, Université de Montréal, Montréal, QC H3C 3J7, Canada.
Ismail El-HamamsyDepartment of Cardiac Surgery, Montréal Heart Institute, Montréal, QC H1T 1C8, Canada.
Marco ColonnaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Goo Taeg OhDepartment of Life Sciences, Ewha Womans University, Seoul 120-750, South Korea. Electronic address: gootaeg@ewha.ac.kr.
Jae-Hoon ChoiDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul 133-791, South Korea. Electronic address: jchoi75@hanyang.ac.kr.
Cheolho CheongLaboratory of Cellular Physiology and Immunology, Institut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada; Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, QC H3A 1A3, Canada; Department of Microbiology, Infectiology, and Immunology, Université de Montréal, Montréal, QC H3C 3J7, Canada. Electronic address: cheolho.cheong@ircm.qc.ca.
Hanyang University · KRMontreal Clinical Research Institute · CAUniversité de Montréal · CAEwha Womans University · KRLudwig-Maximilians-Universität München · DEMcGill University · CAMontreal Heart Institute · CACelldex Therapeutics (United States) · USCentre de Santé et de Services Sociaux Cavendish · CACentre Hospitalier Universitaire Sainte-Justine · CAKorea Research Institute of Bioscience and Biotechnology · KRSeoul National University Hospital · KRWashington University in St. Louis · US

Funding

CIHR 133050CIHR MOP 111226CIHR MOP 125933CIHR MOP 97943
6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) are unique bone-marrow-derived cells that produce large amounts of type I interferon in response to microbial stimulation. Furthermore, pDCs also promote T cell tolerance in sterile-inflammation conditions. However, the immunomodulatory role of aortic pDCs in atherosclerosis has been poorly understood. Here, we identified functional mouse and human pDCs in the aortic intima and showed that selective, inducible pDC depletion in mice exacerbates atherosclerosis. Aortic pDCs expressed CCR9 and indoleamine 2,3-dioxygenase 1 (IDO-1), an enzyme involved in driving the generation of regulatory T cells (Tregs). As a consequence, loss of pDCs resulted in decreased numbers of Tregs and reduced IL-10 levels in the aorta. Moreover, antigen presentation by pDCs expanded antigen-specific Tregs in the atherosclerotic aorta. Notably, Tregs ablation affected pDC homeostasis in diseased aorta. Accordingly, pDCs in human atherosclerotic aortas colocalized with Tregs. Collectively, we identified a mechanism of atheroprotection mediated by tolerogenic aortic pDCs.

Indexed as

AnimalsAntibodiesAortaAtherosclerosisBone MarrowCell CountCell ProliferationDendritic CellsEpitopesfms-Like Tyrosine Kinase 3HomeostasisHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon Type IMacrophagesMembrane ProteinsAntibodiesEpitopesflt3 ligand proteinFlt3 protein, mousefms-Like Tyrosine Kinase 3Indoleamine-Pyrrole 2,3,-DioxygenaseInterferon Type IMembrane ProteinsReceptors, LDLToll-Like Receptor 9

Identifiers

PMID27166946
OpenAlexW2378020047

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.