Evidence map›Paper›PMID 36732946›Full record

ArticleCell reports2023

Ablation of Adar1 in myeloid cells imprints a global antiviral state in the lung and heightens early immunity against SARS-CoV-2.

Julia Z Adamska, Rohit Verma, Shakti Gupta, Thomas Hagan, Florian Wimmers, Katharine Floyd, Qin Li, Erika V Valore, Yanli Wang, Meera Trisal and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
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 5 institutions in 2 countries.

Julia Z AdamskaInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford University, Stanford, CA 94304, USA; Department of Genetics, Stanford University, Stanford, CA 94305, USA.
Rohit VermaInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford University, Stanford, CA 94304, USA.
Shakti GuptaDepartment of Bioengineering, University of California, San Diego, San Diego, CA 92093, USA.
Thomas HaganDivision of Infectious Diseases, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Florian WimmersInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford University, Stanford, CA 94304, USA.
Katharine FloydDepartment of Pediatrics, Department of Microbiology and Immunology, Emory Vaccine Center, Emory National Primate Center, Emory School of Medicine, Atlanta, GA 30329, USA.
Qin LiDepartment of Genetics, Stanford University, Stanford, CA 94305, USA.
Erika V ValoreInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford University, Stanford, CA 94304, USA.
Yanli WangInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford University, Stanford, CA 94304, USA.
Meera TrisalInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford University, Stanford, CA 94304, USA.
José G Vilches-MoureDepartment of Comparative Medicine, Stanford University, Stanford, CA 94305, USA.
Shankar SubramaniamDepartment of Bioengineering, University of California, San Diego, San Diego, CA 92093, USA.
Carl R WalkleySt. Vincent's Institute of Medical Research, Fitzroy, VIC 3065, Australia; Department of Medicine, St. Vincent's Hospital, University of Melbourne, Fitzroy, VIC 3065, Australia.
Mehul S SutharDepartment of Pediatrics, Department of Microbiology and Immunology, Emory Vaccine Center, Emory National Primate Center, Emory School of Medicine, Atlanta, GA 30329, USA.
Jin Billy LiDepartment of Bioengineering, University of California, San Diego, San Diego, CA 92093, USA.
Bali PulendranInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford University, Stanford, CA 94304, USA; Department of Pathology, Stanford University, Stanford, CA 94305, USA; Department of Microbiology & Immunology, Stanford University, Stanford, CA 94305, USA. Electronic address: bpulend@stanford.edu.
Stanford University · USUniversity of California San Diego · USEmory and Henry College · USCincinnati Children's Hospital Medical Center · USThe University of Melbourne · AU

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
Systems Biological Analysis of Innate and Adaptive Responses to VaccinationU19AI090023 · NIAID · EMORY UNIVERSITY · PI AHMED, RAFI, LI, SHUZHAO · 2010 to 2021
$45.0M
MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Systems biological assessment of T cell responses to vaccinationU19AI167903 · NIAID · STANFORD UNIVERSITY · PI BALI PULENDRAN · 2022 to 2026
$13.2M
Vaccine against HCV in nonhuman primatesU19AI159840 · NIAID · STANFORD UNIVERSITY · PI FOUNG, STEVEN · 2021 to 2025
$11.9M
MICROBES, DENDRITIC CELL SUBSETS AND T-CELL IMMUNITYR01AI048638 · NIAID · STANFORD UNIVERSITY · PI PULENDRAN, BALI · 2001 to 2024
$4.5M
Understanding the Role of Mucosal Antigen Presenting Cells in Regulating Immune ResponseR37AI048638 · NIAID · STANFORD UNIVERSITY · PI PULENDRAN, BALI · 2009 to 2018
$4.0M
Polarizing T Cell Responses in vivo With Dendritic CellsR37DK057665 · NIDDK · STANFORD UNIVERSITY · PI PULENDRAN, BALI · 2010 to 2019
$3.9M
NIAID NIH HHS R01 AI048638NIAID NIH HHS R37 AI048638NIAID NIH HHS T32 AI007290NIAID NIH HHS U19 AI057266NIAID NIH HHS U19 AI090023NIAID NIH HHS U19 AI159840NIAID NIH HHS U19 AI167903NIDDK NIH HHS R37 DK057665NIH HHS P51 OD011132
6 · The paper itself

Abstract

Under normal homeostatic conditions, self-double-stranded RNA (self-dsRNA) is modified by adenosine deaminase acting on RNA 1 (ADAR1) to prevent the induction of a type I interferon-mediated inflammatory cascade. Antigen-presenting cells (APCs) sense pathogen-associated molecular patterns, such as dsRNA, to activate the immune response. The impact of ADAR1 on the function of APCs and the consequences to immunity are poorly understood. Here, we show that ADAR1 deletion in CD11c+ APCs leads to (1) a skewed myeloid cell compartment enriched in inflammatory cDC2-like cells, (2) enhanced numbers of activated tissue resident memory T cells in the lung, and (3) the imprinting of a broad antiviral transcriptional signature across both immune and non-immune cells. The resulting changes can be partially reversed by blocking IFNAR1 signaling and promote early resistance against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Our study provides insight into the consequences of self-dsRNA sensing in APCs on the immune system.

Indexed as

COVID-19SARS-CoV-2Adenosine DeaminaseAntiviral AgentsHumansLungMyeloid CellsRNA, Double-StrandedAdenosine DeaminaseAntiviral AgentsRNA, Double-StrandedADAR1CP: Immunologydendritic cellsSARS-CoV-2

Identifiers

PMID36732946
PMCPMC9842623
OpenAlexW4316810328

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.