Evidence map›Paper›PMID 24756110›Full record

ArticleThe Journal of investigative dermatology2014

Natural killer T cells are essential for the development of contact hypersensitivity in BALB/c mice.

Chihiro Shimizuhira, Atsushi Otsuka, Tetsuya Honda, Akihiko Kitoh, Gyohei Egawa, Saeko Nakajima, Chisa Nakashima, Hiroshi Watarai, Yoshiki Miyachi, Kenji Kabashima

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In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Contact dermatitis.Nature reviews. Disease primers · 2021
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Novel concept of iSALT (inducible skin-associated lymphoid tissue) in the elicitation of allergic contact dermatitis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2016
    Review
  15. Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Chihiro ShimizuhiraDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Atsushi OtsukaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. Electronic address: otsukamn@kuhp.kyoto-u.ac.jp.
Tetsuya HondaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Akihiko KitohDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Gyohei EgawaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Saeko NakajimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Chisa NakashimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiroshi WataraiPRESTO, Japan Science and Technology Agency, Tokyo, Japan; Center for Stem Cell Therapy, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Yoshiki MiyachiDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kenji KabashimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kyoto University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Contact hypersensitivity (CHS) has been widely used to study cutaneous immune responses, as a prototype of delayed-type hypersensitivity. Although natural killer T (NKT) cells have been assumed to have an important role in CHS, their role is controversial. Here, we report the role of NKT cells in the sensitization phase of CHS, by promoting the survival and maturation of dendritic cells (DCs) in the draining lymph nodes (LNs). The CHS response was attenuated with Cd1d1(-/-) and Traj18(-/-) BALB/c mice in which NKT cells were absent. In the draining LNs, the number of effector T cells and cytokine production were significantly reduced with NKT cell-deficient mice. NKT cells activated and colocalized with DCs in the draining LNs after sensitization. The number of migrated and mature DCs was reduced in NKT cell-deficient mice 72 hours after FITC application. In in vitro experiments, activated NKT cells enhanced bone marrow-derived DC (BMDC) survivability via tumor necrosis factor (TNF) production from BMDCs. In addition, TNF production from BMDCs was partially suppressed by the neutralizing anti-CD54 or CD154 antibodies. Our data demonstrate that DC-NKT interaction has a pivotal role in the sensitization phase of CHS.

Indexed as

AnimalsApoptosisBone Marrow CellsCell MovementCell ProliferationCell SurvivalCoculture TechniquesCytokinesDendritic CellsDermatitis, ContactFemaleMiceMice, Inbred BALB CNatural Killer T-CellsTumor Necrosis Factor-alphaCytokinesTumor Necrosis Factor-alpha

Identifiers

PMID24756110
OpenAlexW2025346638

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.