Evidence map›Paper›PMID 26438363›Full record

ArticleThe Journal of experimental medicine2015

Resolvin E1 inhibits dendritic cell migration in the skin and attenuates contact hypersensitivity responses.

Yu Sawada, Tetsuya Honda, Sho Hanakawa, Satoshi Nakamizo, Teruasa Murata, Yuri Ueharaguchi-Tanada, Sachiko Ono, Wataru Amano, Saeko Nakajima, Gyohei Egawa and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 104 citations in OpenAlex.

  1. Trial
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  6. Review
  7. Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025
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  8. Generalized Pustular Psoriasis and Systemic Organ Dysfunctions.International journal of molecular sciences · 2024
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  9. The Roles of sPLABiomolecules · 2023
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  14. Maresin-1 and Inflammatory Disease.International journal of molecular sciences · 2022
    Review
  15. Lifestyle Factors Involved in the Pathogenesis of Alopecia Areata.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

4 more citing papers are in PubMed but not listed here.

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

21 authors at 5 institutions in 1 country.

Yu SawadaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan Department of Dermatology, University of Occupational and Environmental Health, Kitakyushu, Fukuoka 807-8555, Japan.
Tetsuya HondaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan Department of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan hontetsu@kuhp.kyoto-u.ac.jp kaba@kuhp.kyoto-u.ac.jp.
Sho HanakawaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Satoshi NakamizoDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Teruasa MurataDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Yuri Ueharaguchi-TanadaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Sachiko OnoDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Wataru AmanoDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Saeko NakajimaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Gyohei EgawaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Hideaki TanizakiDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Atsushi OtsukaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Akihiko KitohDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Teruki DainichiDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Narihito OgawaDepartment of Biomolecular Engineering, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Meguro-ku, Tokyo 152-8550, Japan.
Yuichi KobayashiDepartment of Biomolecular Engineering, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Meguro-ku, Tokyo 152-8550, Japan.
Takehiko YokomizoDepartment of Biochemistry, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan.
Makoto AritaPRESTO, Japan Science and Technology Agency, Chiyoda-ku, Tokyo 102-0076, Japan Laboratory for Metabolomics, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa 230-0045, Japan Graduate School of Medical Life Science, Yokohama City University, Kanazawa-ku, Yokohama 236-0027, Japan.
Motonobu NakamuraDepartment of Dermatology, University of Occupational and Environmental Health, Kitakyushu, Fukuoka 807-8555, Japan.
Yoshiki MiyachiDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan.
Kenji KabashimaDepartment of Dermatology and Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8501, Japan PRESTO, Japan Science and Technology Agency, Chiyoda-ku, Tokyo 102-0076, Japan hontetsu@kuhp.kyoto-u.ac.jp kaba@kuhp.kyoto-u.ac.jp.
Kyoto University · JPJapan Science and Technology Agency · JPTokyo Institute of Technology · JPJuntendo University · JPUniversity of Occupational and Environmental Health Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resolvin E1 (RvE1) is a lipid mediator derived from ω3 polyunsaturated fatty acids that exerts potent antiinflammatory roles in several murine models. The antiinflammatory mechanism of RvE1 in acquired immune responses has been attributed to attenuation of cytokine production by dendritic cells (DCs). In this study, we newly investigated the effect of RvE1 on DC motility using two-photon microscopy in a contact hypersensitivity (CHS) model and found that RvE1 impaired DC motility in the skin. In addition, RvE1 attenuated T cell priming in the draining lymph nodes and effector T cell activation in the skin, which led to the reduced skin inflammation in CHS. In contrast, leukotriene B4 (LTB4) induced actin filament reorganization in DCs and increased DC motility by activating Cdc42 and Rac1 via BLT1, which was abrogated by RvE1. Collectively, our results suggest that RvE1 attenuates cutaneous acquired immune responses by inhibiting cutaneous DC motility, possibly through LTB4-BLT1 signaling blockade.

Indexed as

ActinsAnimalsCell MovementCells, CulturedDendritic CellsDermatitis, ContactEicosapentaenoic AcidFemaleInterferon-gammaLeukotriene B4MiceMice, Inbred C57BLReceptors, Leukotriene B4Skin5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acidActinsEicosapentaenoic AcidInterferon-gammaLeukotriene B4Ltb4r1 protein, mouseReceptors, Leukotriene B4

Identifiers

PMID26438363
PMCPMC4612099
OpenAlexW2178888160

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.