Evidence map›Paper›PMID 33761354›Full record

ArticleCell reports2021

IRF1 governs the differential interferon-stimulated gene responses in human monocytes and macrophages by regulating chromatin accessibility.

Ran Song, Yajing Gao, Igor Dozmorov, Venkat Malladi, Irene Saha, Margaret M McDaniel, Sreeja Parameswaran, Chaoying Liang, Carlos Arana, Bo Zhang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.7field-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

60 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Review
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  5. Tenofovir, Interferon Pathways, and Mucosal Immunity: Implications for People Living With HIV.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Review
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  16. Frontiers in immunology · 2026
    Article
  17. Article
  18. Article
  19. 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

16 authors at 3 institutions in 1 country.

Ran SongDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Yajing GaoDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Igor DozmorovDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Venkat MalladiBioinformatics Core Facility, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Irene SahaDivision of Immunobiology and Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Margaret M McDanielDivision of Immunobiology and Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Immunology Graduate Program, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Sreeja ParameswaranCenter for Autoimmune Genetics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Chaoying LiangDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Carlos AranaDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Bo ZhangDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Benjamin WakelandDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Jinchun ZhouDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Matthew T WeirauchCenter for Autoimmune Genetics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Divisions of Biomedical Informatics and Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Leah C KottyanDivision of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Center for Autoimmune Genetics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Edward K WakelandDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: ward.wakeland@utsouthwestern.edu.
Chandrashekhar PasareDivision of Immunobiology and Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA. Electronic address: chandrashekhar.pasare@cchmc.org.
The University of Texas Southwestern Medical Center · USCincinnati Children's Hospital Medical Center · USSouthwestern Medical Center · US

Funding

INTEGRATIVE IMMUNOLOGY TRAINING PROGRAMT32AI005284 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Nan Yan · 2003 to 2026
$7.4M
BIOCHEMICAL AND GENETIC ANALYSIS OF NOTCH SIGNALINGR01GM055479 · NIGMS · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL, WEIRAUCH, MATTHEW TYSON · 1996 to 2021
$6.4M
Innate mechanisms of regulation of Th17 responsesR01AI123176 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Chandrashekhar Pasare · 2017 to 2026
$4.4M
Binding of Epstein Barr Virus EBNA2 Unifies Multiple Sclerosis Genetic MechanismsR01NS099068 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI Leah Claire Kottyan, Matthew Tyson Weirauch · 2017 to 2026
$4.2M
Genomics of Inflammatory Bowel DiseaseR01AI148276 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI KOTTYAN, LEAH CLAIRE · 2019 to 2023
$3.9M
Role of Gut Microbiota in Modulating Immune Checkpoint Inhibitory Therapy for CancerR01CA231303 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HOMSI, JADE, KOH, ANDREW · 2019 to 2023
$3.1M
Virus-driven human gene misregulation in diseaseR01HG010730 · NHGRI · CINCINNATI CHILDRENS HOSP MED CTR · PI WEIRAUCH, MATTHEW TYSON · 2020 to 2023
$2.7M
Transcription Factor Genetics in LupusR01AR073228 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI KOTTYAN, LEAH CLAIRE, WAGGONER, STEPHEN N. · 2019 to 2023
$2.2M
ROLE OF BCAP IN REGULATING INFLAMMATION AND ADAPTIVE IMMUNITYR01AI113125 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI PASARE, CHANDRASHEKHAR · 2015 to 2019
$1.8M
Mechanisms of genetic risk at 2p23 in Eosinophilic EsophagitisR01DK107502 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI KOTTYAN, LEAH CLAIRE · 2016 to 2020
$1.8M
Endocytic Trafficking and Cell Signaling in Models of ARC SyndromeR01GM120196 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI KRAMER, HELMUT J · 2017 to 2020
$1.3M
Mentoring Patient Oriented Research in the Microbiome of Cancer and Stem Cell Transplant PatientsK24AI150992 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI KOH, ANDREW · 2020 to 2024
$592k
NCI NIH HHS R01 CA231303NHGRI NIH HHS R01 HG010730NIAID NIH HHS K24 AI150992NIAID NIH HHS R01 AI113125NIAID NIH HHS R01 AI123176NIAID NIH HHS R01 AI148276NIAID NIH HHS T32 AI005284NIAMS NIH HHS R01 AR073228NIDDK NIH HHS R01 DK107502NIGMS NIH HHS R01 GM055479NIGMS NIH HHS R01 GM120196NINDS NIH HHS R01 NS099068
6 · The paper itself

Abstract

Myeloid lineage cells use TLRs to recognize and respond to diverse microbial ligands. Although unique transcription factors dictate the outcome of specific TLR signaling, whether lineage-specific differences exist to further modulate the quality of TLR-induced inflammation remains unclear. Comprehensive analysis of global gene transcription in human monocytes, monocyte-derived macrophages, and monocyte-derived dendritic cells stimulated with various TLR ligands identifies multiple lineage-specific, TLR-responsive gene programs. Monocytes are hyperresponsive to TLR7/8 stimulation that correlates with the higher expression of the receptors. While macrophages and monocytes express similar levels of TLR4, macrophages, but not monocytes, upregulate interferon-stimulated genes (ISGs) in response to TLR4 stimulation. We find that TLR4 signaling in macrophages uniquely engages transcription factor IRF1, which facilitates the opening of ISG loci for transcription. This study provides a critical mechanistic basis for lineage-specific TLR responses and uncovers IRF1 as a master regulator for the ISG transcriptional program in human macrophages.

Indexed as

Gene Expression RegulationBase SequenceCell LineageCell NucleusChemokinesChromatinDendritic CellsHumansImmunityInterferon Regulatory Factor-1InterferonsLipopolysaccharidesMacrophagesMonocytesMyeloid CellsNucleotide MotifsChemokinesChromatinInterferon Regulatory Factor-1InterferonsLipopolysaccharidesToll-Like Receptorschromatin accessibilityhuman PBMCsinterferon-stimulated genesIRF1IRF3macrophagesmonocytespioneer transcription factorTLR4TLR8

Identifiers

PMID33761354
PMCPMC8300000
OpenAlexW3138049691

What OpenQuestion holds

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Read underepoch 390

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.