Evidence map›Paper›PMID 31464028›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2020

Role of Interferon-γ-Producing Th1 Cells in a Murine Model of Type I Interferon-Independent Autoinflammation Resulting From DNase II Deficiency.

Sudesh Pawaria, Kerstin Nündel, Kevin M Gao, Stephanie Moses, Patricia Busto, Kevin Holt, Rohit B Sharma, Michael A Brehm, Ellen M Gravallese, Merav Socolovsky and 2 more

Open access · greenAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. STING and liver disease.Journal of gastroenterology · 2021
    Review
  6. Article
  7. Article
  8. 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

12 authors at 2 institutions in 2 countries.

Sudesh PawariaUniversity of Massachusetts Medical School, Worcester.
Kerstin NündelUniversity of Massachusetts Medical School, Worcester.
Kevin M GaoUniversity of Massachusetts Medical School, Worcester.
Stephanie MosesUniversity of Massachusetts Medical School, Worcester.
Patricia BustoUniversity of Massachusetts Medical School, Worcester.
Kevin HoltUniversity of Massachusetts Medical School, Worcester.
Rohit B SharmaUniversity of Massachusetts Medical School, Worcester.
Michael A BrehmUniversity of Massachusetts Medical School, Worcester.
Ellen M GravalleseUniversity of Massachusetts Medical School, Worcester.
Merav SocolovskyUniversity of Massachusetts Medical School, Worcester.
Anette ChristUniversity Hospital Bonn, Bonn, Germany.
Ann Marshak-RothsteinUniversity of Massachusetts Medical School, Worcester.ORCID 0000-0003-2136-8130
University of Massachusetts Chan Medical School · USUniversity Hospital Bonn · DE

Funding

Novel humanized mouse model developed from cord blood CD34 positive HSC and autologous iPS cell derived thymusR01AI132963 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BREHM, MICHAEL ALLEN, MAEHR, RENE · 2017 to 2021
$4.4M
Regulation of Lupus by Cytosolic DNA SensorsR01AI128358 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FITZGERALD, KATHERINE A., MARSHAK-ROTHSTEIN, ANN · 2017 to 2021
$2.7M
Distinct Functional Outcomes of BCR/TLR7 and BCR/TLR9 Co-engagementR01AR066808 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 2015 to 2019
$2.6M
Training in the Molecular Basis of Autoimmunity and AutoinflammationT32AI132152 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Katherine A. Fitzgerald, Ann Marshak-Rothstein · 2018 to 2026
$1.6M
NIAID NIH HHS R01 AI128358NIAID NIH HHS R01 AI132963NIAID NIH HHS T32 AI132152NIAMS NIH HHS AR066808NIAMS NIH HHS R01 AR066808
6 · The paper itself

Abstract

objectivePatients with hypomorphic mutations in DNase II develop a severe and debilitating autoinflammatory disease. This study was undertaken to compare the disease parameters in these patients to those in a murine model of DNase II deficiency, and to evaluate the role of specific nucleic acid sensors and identify the cell types responsible for driving the autoinflammatory response.

methodsTo avoid embryonic death, Dnase2

resultsIn Dnase2

conclusionDnase2

Indexed as

AnimalsAutoimmune DiseasesDisease Models, AnimalEndodeoxyribonucleasesInflammationInterferon-gammaInterferon Type IMiceMice, Inbred C57BLTh1 Cellsdeoxyribonuclease IIEndodeoxyribonucleasesInterferon-gammaInterferon Type I

Identifiers

PMID31464028
PMCPMC6994331
OpenAlexW2970953251

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.