Evidence map›Paper›PMID 23365081›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Activation of invariant NK T cells in periodontitis lesions.

Michael Nowak, Benjamin Krämer, Manuela Haupt, Panos N Papapanou, Justus Kebschull, Per Hoffmann, Ingo G Schmidt-Wolf, Søren Jepsen, Peter Brossart, Sven Perner and 1 more

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. The Epidermal Transcriptome Analysis of a Novel c.639_642dupInternational journal of molecular sciences · 2023
    Article
  4. Article
  5. Review
  6. Review
  7. The influence ofCentral-European journal of immunology · 2017
    Article
  8. Genome-Wide Analysis of Periodontal and Peri-Implant Cells and Tissues.Methods in molecular biology (Clifton, N.J.) · 2017
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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

11 authors.

Michael NowakDepartment of Prostate Cancer Research, Institute of Pathology, University of Bonn, Bonn 53127, Germany. nowakm@uni-bonn.de
Benjamin Krämer
Manuela Haupt
Panos N Papapanou
Justus Kebschull
Per Hoffmann
Ingo G Schmidt-Wolf
Søren Jepsen
Peter Brossart
Sven Perner
Moritz Kebschull

Funding

Gene Expression in Chronic and Aggressive PeriodontitisR01DE015649 · NIDCR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PAPAPANOU, PANOS N · 2004 to 2006
$1.8M
MicroRNA expression in gingival tissues in periodontal health and diseaseR21DE021820 · NIDCR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PAPAPANOU, PANOS N · 2012 to 2013
$432k
NIDCR NIH HHS R01 DE015649NIDCR NIH HHS R21 DE021820
6 · The paper itself

Abstract

Periodontitis is one of the most prevalent human inflammatory diseases. The major clinical phenotypes of this polymicrobial, biofilm-mediated disease are chronic and aggressive periodontitis, the latter being characterized by a rapid course of destruction that is generally attributed to an altered immune-inflammatory response against periodontal pathogens. Still, the biological basis for the pathophysiological distinction of the two disease categories has not been well documented yet. Type I NKT cells are a lymphocyte subset with important roles in regulating immune responses to either tolerance or immunity, including immune responses against bacterial pathogens. In this study, we delineate the mechanisms of NKT cell activation in periodontal infections. We show an infiltration of type I NKT cells in aggressive, but not chronic, periodontitis lesions in vivo. Murine dendritic cells infected with aggressive periodontitis-associated Aggregatibacter actinomycetemcomitans triggered a type I IFN response followed by type I NKT cell activation. In contrast, infection with Porphyromonas gingivalis, a principal pathogen in chronic periodontitis, did not induce NKT cell activation. This difference could be explained by the absence of a type I IFN response to P. gingivalis infection. We found these IFNs to be critical for NKT cell activation. Our study provides a conceivable biological distinction between the two periodontitis subforms and identifies factors required for the activation of the immune system in response to periodontal bacteria.

Indexed as

Host-Pathogen InteractionsAcute DiseaseAdultAggregatibacter actinomycetemcomitansAnimalsBiopsyCell MovementChronic DiseaseDendritic CellsHumansInterferon Type ILymphocyte ActivationMiceMice, KnockoutNatural Killer T-CellsPeriodontitisInterferon Type I

Identifiers

PMID23365081
PMCPMC3620697

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.