Evidence map›Paper›PMID 11290557›Full record

ArticleThe American journal of pathology2001

Elevated proportion of natural killer T cells in periodontitis lesions: a common feature of chronic inflammatory diseases.

K Yamazaki, Y Ohsawa, H Yoshie

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. The influence ofCentral-European journal of immunology · 2017
    Article
  7. Langerhans cells down-regulate inflammation-driven alveolar bone loss.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  8. Review
  9. 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

3 authors at 1 institution in 1 country.

K YamazakiDepartment of Periodontology, Faculty of Dentistry, Niigata University, 5274, Gakkocho-Dori 2-ban-cho, Niigata 951-8514, Japan. kaz@dent.niigata-u.ac.jp
Y Ohsawa
H Yoshie
Niigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although periodontitis is a chronic inflammatory disease caused by a group of so-called periodontopathic bacteria, autoimmune mechanisms have also been implicated in the disease process. Recently, a unique subset of lymphocytes designated natural killer (NK) T cells expressing the Valpha24JalphaQ invariant T cell receptor (TCR) has been reported to have a regulatory role in certain autoimmune diseases. Therefore, we investigated the proportion of the invariant Valpha24JalphaQ TCR within the Valpha24 T cell population in periodontitis lesions and gingivitis lesions using single-strand conformation polymorphism methodology. NK T cells were identified with a specific JalphaQ probe whereas the total Valpha24 TCR was identified using an internal Calpha probe. NK T cells were a significant proportion of the total Valpha24 population both in periodontitis lesions and to a lesser extent in gingivitis lesions but not in the peripheral blood of either periodontitis patients or nondiseased controls. Using immunohistochemistry, some of Valpha24(+) cells in the periodontitis lesions seemed to associate with CD1d(+) cells, which are specific antigen-presenting cells for NK T cells. Although the mechanism underlying the elevation of NK T cells in periodontitis and in gingivitis lesions remains unclear, it can be postulated that NK T cells are recruited to a play regulatory role in the immune response to bacterial infection.

Indexed as

AdultAntigens, CD1Antigens, CD1dChronic DiseaseClone CellsGenetic VariationGingivaHumansImmunohistochemistryInflammationKiller Cells, NaturalMiddle AgedPeriodontitisReceptors, Antigen, T-CellT-LymphocytesAntigens, CD1Antigens, CD1dCD1D protein, humanReceptors, Antigen, T-Cell

Identifiers

PMID11290557
PMCPMC1891892
OpenAlexW92103573

What OpenQuestion holds

Textmetadata
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.