Evidence map›Paper›PMID 25112380›Full record

ArticleScientific reports2014

Tracking and quantification of dendritic cell migration and antigen trafficking between the skin and lymph nodes.

Michio Tomura, Akihiro Hata, Satoshi Matsuoka, Francis H W Shand, Yasutaka Nakanishi, Ryoyo Ikebuchi, Satoshi Ueha, Hidekazu Tsutsui, Kayo Inaba, Kouji Matsushima and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
–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

111 citing papers in PubMed.

  1. CD4Oncoimmunology · 2026
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  5. M cell-dependent commensal uptake confers encephalitogenic phenotypes on γδT17 cells in Peyer's patches.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Article
  19. Understanding the Lymphatic System: Tissue-on-Chip Modeling.Annual review of biomedical engineering · 2025
    Review
  20. Review

51 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

14 authors.

Michio Tomura1] Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan [2] Laboratory for Autoimmune Regulation, Research Center for Allergy and Immunology, RIKEN, 1-7-22 Suehiro-cho, Tsurumi, Yokohama City, Kanagawa 230-0045, Japan [3] Department of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3- 1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Akihiro HataCenter for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan.
Satoshi Matsuoka1] Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan [2].
Francis H W Shand1] Department of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3- 1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan [2] Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville, Victoria 3010, Australia.
Yasutaka NakanishiCenter for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan.
Ryoyo IkebuchiCenter for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan.
Satoshi UehaDepartment of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3- 1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Hidekazu TsutsuiLaboratory for Cell Function and Dynamics, Advanced Technology Development Center, Brain Science Institute, RIKEN.
Kayo InabaLaboratory of Immunobiology, Department of Animal Development and Physiology, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan.
Kouji MatsushimaDepartment of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3- 1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Atsushi Miyawaki1] Laboratory for Cell Function and Dynamics, Advanced Technology Development Center, Brain Science Institute, RIKEN [2] Life Function and Dynamics, ERATO, JST, 2-1 Hirosawa, Wako City, Saitama 351-0198, Japan.
Kenji KabashimaDepartment of Dermatology, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawara, Kyoto 606-8501, Japan.
Takeshi Watanabe1] Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Kyoto 606-8501, Japan [2].
Osami Kanagawa1] Department of Molecular Preventive Medicine, Graduate School of Medicine, The University of Tokyo, 7-3- 1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan [2].

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skin-derived dendritic cells (DCs) play a crucial role in the maintenance of immune homeostasis due to their role in antigen trafficking from the skin to the draining lymph nodes (dLNs). To quantify the spatiotemporal regulation of skin-derived DCs in vivo, we generated knock-in mice expressing the photoconvertible fluorescent protein KikGR. By exposing the skin or dLN of these mice to violet light, we were able to label and track the migration and turnover of endogenous skin-derived DCs. Langerhans cells and CD103(+)DCs, including Langerin(+)CD103(+)dermal DCs (DDCs), remained in the dLN for 4-4.5 days after migration from the skin, while CD103(-)DDCs persisted for only two days. Application of a skin irritant (chemical stress) induced a transient >10-fold increase in CD103(-)DDC migration from the skin to the dLN. Tape stripping (mechanical injury) induced a long-lasting four-fold increase in CD103(-)DDC migration to the dLN and accelerated the trafficking of exogenous protein antigens by these cells. Both stresses increased the turnover of CD103(-)DDCs within the dLN, causing these cells to die within one day of arrival. Therefore, CD103(-)DDCs act as sentinels against skin invasion that respond with increased cellular migration and antigen trafficking from the skin to the dLNs.

Indexed as

AnimalsAntigens, CDCell MovementDendritic CellsDermatitis, IrritantGene Knock-In TechniquesIntegrin alpha ChainsLangerhans CellsLightLymph NodesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, FluorescenceProteinsalpha E integrinsAntigens, CDCcr7 protein, mouseIntegrin alpha ChainsProteinsReceptors, CCR7ROSA22 protein, mouse

Identifiers

PMID25112380
PMCPMC4129424

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Registered trials

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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.