Evidence map›Paper›PMID 30873168›Full record

ArticleFrontiers in immunology2019

Rapid Downregulation of DAB2 by Toll-Like Receptor Activation Contributes to a Pro-Inflammatory Switch in Activated Dendritic Cells.

Vanessa Figliuolo da Paz, Deepa R Jamwal, Michael Gurney, Monica Midura-Kiela, Christy A Harrison, Christopher Cox, Jean M Wilson, Fayez K Ghishan, Pawel R Kiela

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. 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
1.5field-weighted citation impact, top 18% 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, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Proinflammatory CD14Infection and immunity · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Disabled-2 (International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Endocytic Adaptors in Cardiovascular Disease.Frontiers in cell and developmental biology · 2020
    Review
  15. 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

9 authors at 1 institution in 1 country.

Vanessa Figliuolo da PazDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States.
Deepa R JamwalDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States.
Michael GurneyDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States.
Monica Midura-KielaDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States.
Christy A HarrisonDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States.
Christopher CoxDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Jean M WilsonDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Fayez K GhishanDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States.
Pawel R KielaDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States.
University of Arizona · US

Funding

Endocytic Regulation of Intestinal DevelopmentR01DK109701 · NIDDK · UNIVERSITY OF ARIZONA · PI WILSON, JEAN M · 2017 to 2021
$2.1M
Modulation of dendritic cell function in the pathogenesis of Inflammatory Bowel DiseasesR01DK109711 · NIDDK · UNIVERSITY OF ARIZONA · PI GHISHAN, FAYEZ KHALAF, KIELA, PAWEL R · 2016 to 2020
$1.7M
NIDDK NIH HHS R01 DK109701NIDDK NIH HHS R01 DK109711
6 · The paper itself

Abstract

Dendritic cells (DCs) are pivotal in regulating tolerogenic as well as immunogenic responses against microorganisms by directing both the innate and adaptive immune response. In health, phenotypically different DC subsets found in the gut mucosa are maintained in their tolerogenic state but switch to a pro-inflammatory phenotype during infection or chronic autoinflammatory conditions such as inflammatory bowel disease (IBD). The mechanisms that promote the switch among the mucosal DCs from a tolerogenic to an immunogenic, pro-inflammatory phenotype are incompletely understood. We hypothesized that disabled homolog 2 (DAB2), recently described as a negative regulator of DC immunogenicity during their development, is regulated during intestinal inflammation and modulates mucosal DC function. We show that DAB2 is highly expressed in colonic CD11b

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsColitisDendritic CellsDown-RegulationHumansLipopolysaccharidesMaleMice, Inbred C57BLMice, TransgenicPhagocytosisToll-Like ReceptorsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsDab2 protein, mouseLipopolysaccharidesToll-Like ReceptorscolonDab2dendritic cellsimmunoregulationinflammationsmall intestine

Identifiers

PMID30873168
PMCPMC6400992
OpenAlexW2915743535

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.