Evidence map›Paper›PMID 29760532›Full record

ArticleNature immunology2018

Apoptotic cell-induced AhR activity is required for immunological tolerance and suppression of systemic lupus erythematosus in mice and humans.

Rahul Shinde, Kebria Hezaveh, Marie Jo Halaby, Andreas Kloetgen, Ankur Chakravarthy, Tiago da Silva Medina, Reema Deol, Kieran P Manion, Yuriy Baglaenko, Maria Eldh and 14 more

Abstract read
In one paragraph

Article in Nature immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

133 citing papers in PubMed, 194 citations in OpenAlex.

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  5. [Role of AHR-mediated histone acetylation at FOXP3 in Tfr cell differentiation in systemic lupus erythematosus].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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73 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 8 institutions in 3 countries.

Rahul ShindeTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.ORCID http://orcid.org/0000-0001-8767-5032
Kebria HezavehTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Marie Jo HalabyTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Andreas KloetgenDepartment of Pathology, New York University School of Medicine, New York, NY, USA.
Ankur ChakravarthyDepartment of Medical Biophysics, University of Toronto, Toronto, ON, Canada.
Tiago da Silva MedinaTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Reema DeolTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Kieran P ManionDepartment of Immunology, University of Toronto, Toronto, ON, Canada.
Yuriy BaglaenkoDepartment of Immunology, University of Toronto, Toronto, ON, Canada.
Maria EldhDepartment of Medicine, Unit for Immunology and Allergy, Karolinska Institute, Stockholm, Sweden.
Sara LamorteTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Drew WallaceTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Sathi Babu ChodisettiDepartment of Immunology, Pennsylvania State University School of Medicine, Hershey, PA, USA.
Buvana RavishankarDepartment of Cancer Immunology, Genentech, San Francisco, CA, USA.
Haiyun LiuDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Kapil ChaudharyDepartment of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
David H MunnDepartment of Paediatrics, Medical College of Georgia, Augusta, GA, USA.
Aristotelis TsirigosDepartment of Pathology, New York University School of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0002-7512-8477
Michael MadaioDepartment of Medicine, Medical College of Georgia, Augusta, GA, USA.
Susanne GabrielssonDepartment of Medicine, Unit for Immunology and Allergy, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-1771-1346
Zahi ToumaUniversity of Toronto Lupus Clinic, University of Toronto, Toronto, ON, Canada.
Joan WitherDepartment of Immunology, University of Toronto, Toronto, ON, Canada.
Daniel D De CarvalhoTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Tracy L McGahaTumor Immunotherapy Program, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. tmcgaha@uhnresearch.ca.ORCID http://orcid.org/0000-0003-4721-9301
University Health Network · CAUniversity of Toronto · CAAugusta University · USKarolinska Institutet · SENew York University · USJohns Hopkins University · USPennsylvania State University · USWashington University in St. Louis · US

Funding

Reprogramming the TME for immunogenic antigen-presentationR01CA103320 · NCI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI MUNN, DAVID H. · 2003 to 2024
$6.0M
PTEN, Tregs and MDSCs in the tumor microenvironmentR01CA211229 · NCI · AUGUSTA UNIVERSITY · PI MUNN, DAVID H. · 2017 to 2021
$1.7M
The role of marginal zone macrophages and immuno-metabolism in tumor-driven MDSC developmentR01CA190449 · NCI · UNIVERSITY HEALTH NETWORK · PI MCGAHA, TRACY L · 2015 to 2020
$1.3M
Mechanistic relationships between IDO, GCN2, and mTOR signals in immunity to apoptotic cellsR01AR067763 · NIAMS · UNIVERSITY HEALTH NETWORK · PI MCGAHA, TRACY L · 2015 to 2019
$1.2M
The role of GCN2-kinase in antigen presenting cell function and tolerance to selfR21AI105500 · NIAID · AUGUSTA UNIVERSITY · PI MCGAHA, TRACY L · 2013 to 2014
$399k
NCI NIH HHS R01 CA103320NCI NIH HHS R01 CA190449NCI NIH HHS R01 CA211229NIAID NIH HHS R21 AI105500NIAMS NIH HHS R01 AR067763
6 · The paper itself

Abstract

The transcription factor AhR modulates immunity at multiple levels. Here we report that phagocytes exposed to apoptotic cells exhibited rapid activation of AhR, which drove production of the cytokine IL-10. Activation of AhR was dependent on interactions between apoptotic-cell DNA and the pattern-recognition receptor TLR9 that was required for the prevention of immune responses to DNA and histones in vivo. Moreover, disease progression in mouse systemic lupus erythematosus (SLE) correlated with strength of the AhR signal, and the disease course could be altered by modulation of AhR activity. Deletion of AhR in the myeloid lineage caused systemic autoimmunity in mice, and an enhanced AhR transcriptional signature correlated with disease in patients with SLE. Thus, AhR activity induced by apoptotic cell phagocytes maintains peripheral tolerance.

Indexed as

AnimalsApoptosisHumansImmune ToleranceLupus Erythematosus, SystemicMacrophagesMiceReceptors, Aryl HydrocarbonSignal TransductionToll-Like Receptor 9Receptors, Aryl HydrocarbonToll-Like Receptor 9

Identifiers

PMID29760532
PMCPMC5976527
OpenAlexW2800526280

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.