Evidence map›Paper›PMID 22509018›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Langerhans cells down-regulate inflammation-driven alveolar bone loss.

Moran Arizon, Itay Nudel, Hadas Segev, Gabriel Mizraji, Mazal Elnekave, Karina Furmanov, Luba Eli-Berchoer, Björn E Clausen, Lior Shapira, Asaf Wilensky and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

46 citing papers in PubMed, 74 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Role of regulatory immune cells in pathogenesis and therapy of periodontitis.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Adult Langerhans Cell Histiocytosis and the Skeleton.Journal of clinical medicine · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. RANKL and osteoimmunology in periodontitis.Journal of bone and mineral metabolism · 2021
    Review
  19. Article
  20. 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 at 3 institutions in 3 countries.

Moran ArizonInstitute of Dental Sciences, Hebrew University-Hadassah School of Dental Medicine, Jerusalem 91120, Israel.
Itay Nudel
Hadas Segev
Gabriel Mizraji
Mazal Elnekave
Karina Furmanov
Luba Eli-Berchoer
Björn E Clausen
Lior Shapira
Asaf Wilensky
Avi-Hai Hovav
University of Dental Medicine · MMHebrew University of Jerusalem · ILErasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive bone resorption is frequently associated with chronic infections and inflammatory diseases. Whereas T cells were demonstrated to facilitate osteoclastogenesis in such diseases, the role of dendritic cells, the most potent activators of naive T cells, remains unclear. Using a model involving inflammation-driven alveolar bone loss attributable to infection, we showed that in vivo ablation of Langerhans cells (LCs) resulted in enhanced bone loss. An increased infiltration of B and T lymphocytes into the tissue surrounding the bone was observed in LC-ablated mice, including receptor activator of NF-κB ligand (RANKL)-expressing CD4(+) T cells with known capabilities of altering bone homeostasis. In addition, the absence of LCs significantly reduced the numbers of CD4(+)Foxp3(+) T-regulatory cells in the tissue. Further investigation revealed that LCs were not directly involved in presenting antigens to T cells. Nevertheless, despite their low numbers in the tissue, the absence of LCs resulted in an elevated activation of CD4(+) but not CD8(+) T cells. This activation involved elevated production of IFN-γ but not IL-17 or IL-10 cytokines. Our data, thus, reveal a protective immunoregulatory role for LCs in inflammation-induced alveolar bone resorption, by inhibiting IFN-γ secretion and excessive activation of RANKL(+)CD4(+) T cells with a capability of promoting osteoclastogenesis.

Indexed as

Alveolar Bone LossAnimalsAntigens, CDBacteroidaceae InfectionsBase SequenceCD4-Positive T-LymphocytesDisease Models, AnimalDNA PrimersDown-RegulationHeparin-binding EGF-like Growth FactorHumansInflammationIntercellular Signaling Peptides and ProteinsInterferon-gammaInterleukin-10Interleukin-17Antigens, CDCD207 protein, humanDNA PrimersHBEGF protein, humanHbegf protein, mouseHeparin-binding EGF-like Growth FactorIL10 protein, mouseIntercellular Signaling Peptides and ProteinsInterferon-gammaInterleukin-10Interleukin-17Lectins, C-TypeMannose-Binding LectinsRANK LigandTnfsf11 protein, mouse

Identifiers

PMID22509018
PMCPMC3344981
OpenAlexW1994654042

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.