Evidence map›Paper›PMID 37200107›Full record

ArticleThe Journal of clinical investigation2023

Poly(ADP-ribose) polymerase 9 mediates early protection against Mycobacterium tuberculosis infection by regulating type I IFN production.

Shyamala Thirunavukkarasu, Mushtaq Ahmed, Bruce A Rosa, Mark Boothby, Sung Hoon Cho, Javier Rangel-Moreno, Stanley K Mbandi, Valérie Schreiber, Ananya Gupta, Joaquin Zuniga and 4 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
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  5. Article
  6. Review
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  8. Review
  9. Quantitative Proteomic Analysis of Macrophages Infected withInternational journal of molecular sciences · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Frontiers in immunology · 2024
    Article
  14. Review
  15. 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

14 authors at 7 institutions in 4 countries.

Shyamala ThirunavukkarasuDepartment of Molecular Microbiology.
Mushtaq AhmedDepartment of Molecular Microbiology.
Bruce A RosaMcDonnell Genome Institute, and.
Mark BoothbyDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Sung Hoon ChoDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Javier Rangel-MorenoDepartment of Medicine, Division of Allergy, Immunology, and Rheumatology, University of Rochester Medical Center, Rochester, New York, USA.
Stanley K MbandiSouth African Tuberculosis Vaccine Initiative, Institute of Infectious Disease and Molecular Medicine and Division of Immunology, Department of Pathology, University of Cape Town, Cape Town, South Africa.
Valérie SchreiberBiotechnology and Cell Signaling, CNRS UMR7242, Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS UMR7104, INSERM U1258, Université de Strasbourg, Illkirch, France.
Ananya GuptaDepartment of Molecular Microbiology.
Joaquin ZunigaLaboratory of Immunobiology and Genetics, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Mexico City, Mexico.
Makedonka MitrevaMcDonnell Genome Institute, and.
Deepak KaushalSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, Texas, USA.
Thomas J ScribaSouth African Tuberculosis Vaccine Initiative, Institute of Infectious Disease and Molecular Medicine and Division of Immunology, Department of Pathology, University of Cape Town, Cape Town, South Africa.
Shabaana A KhaderDepartment of Molecular Microbiology.
University of Cape Town · ZAVanderbilt University Medical Center · USWashington University in St. Louis · USCentre National de la Recherche Scientifique · FRInstituto Nacional de Enfermedades Respiratorias · MXTexas Biomedical Research Institute · USUniversity of Rochester Medical Center · US

Funding

The Southwest National Primate Research Center Supplement- Infrastructure improvements of ABSL2 holding areasP51OD011133 · OD · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI Larry S. Schlesinger · 2012 to 2026
$129.7M
Viral Testing CoreU42OD010442 · OD · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI Deepak Kaushal, Kathryn Shelton · 2012 to 2026
$35.6M
ROLE OF INDUCIBLE BRONCHUS ASSOCIATED LYMPHOID TISSUE IN LATENT TUBERCULOSISR01AI111914 · NIAID · WASHINGTON UNIVERSITY · PI KAUSHAL, DEEPAK, KHADER, SHABAANA A. · 2015 to 2025
$11.1M
ROLE OF IL-17 IN PROTECTIVE VACCINE-INDUCED IMMUNE RESPONSES AGAINST TUBERCULOSISR01HL105427 · NHLBI · WASHINGTON UNIVERSITY · PI KHADER, SHABAANA A. · 2011 to 2025
$5.9M
The Role of Group 3 Innate Lymphoid cells (ILC3) in TuberculosisR01AI134236 · NIAID · WASHINGTON UNIVERSITY · PI COLONNA, MARCO, KHADER, SHABAANA A. · 2017 to 2021
$4.4M
COMMON IMMUNE CORRELATES OF RISK OF TB DISEASE IN ANIMAL MODELS AND HUMANSR01AI123780 · NIAID · WASHINGTON UNIVERSITY · PI KAUSHAL, DEEPAK, KHADER, SHABAANA A. · 2016 to 2019
$2.9M
NHLBI NIH HHS R01 HL105427NIAID NIH HHS R01 AI111914NIAID NIH HHS R01 AI123780NIAID NIH HHS R01 AI134236NIH HHS P51 OD011133NIH HHS U42 OD010442
6 · The paper itself

Abstract

The ADP ribosyltransferases (PARPs 1-17) regulate diverse cellular processes, including DNA damage repair. PARPs are classified on the basis of their ability to catalyze poly-ADP-ribosylation (PARylation) or mono-ADP-ribosylation (MARylation). Although PARP9 mRNA expression is significantly increased in progressive tuberculosis (TB) in humans, its participation in host immunity to TB is unknown. Here, we show that PARP9 mRNA encoding the MARylating PARP9 enzyme was upregulated during TB in humans and mice and provide evidence of a critical modulatory role for PARP9 in DNA damage, cyclic GMP-AMP synthase (cGAS) expression, and type I IFN production during TB. Thus, Parp9-deficient mice were susceptible to Mycobacterium tuberculosis infection and exhibited increased TB disease, cGAS and 2'3'-cyclic GMP-AMP (cGAMP) expression, and type I IFN production, along with upregulation of complement and coagulation pathways. Enhanced M. tuberculosis susceptibility is type I IFN dependent, as blockade of IFN α receptor (IFNAR) signaling reversed the enhanced susceptibility of Parp9-/- mice. Thus, in sharp contrast to PARP9 enhancement of type I IFN production in viral infections, this member of the MAR family plays a protective role by limiting type I IFN responses during TB.

Indexed as

Mycobacterium tuberculosisTuberculosisADP-RibosylationAnimalsDNA RepairHumansMiceNeoplasm ProteinsNucleotidyltransferasesPoly(ADP-ribose) PolymerasesNeoplasm ProteinsNucleotidyltransferasesPARP9 protein, humanParp9 protein, mousePoly(ADP-ribose) PolymerasesBacterial infectionsImmunologyInfectious diseaseInnate immunityTuberculosis

Identifiers

PMID37200107
PMCPMC10266794
OpenAlexW4377093438

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.