Evidence map›Paper›PMID 25240383›Full record

ArticleNature immunology2014

Perivascular leukocyte clusters are essential for efficient activation of effector T cells in the skin.

Yohei Natsuaki, Gyohei Egawa, Satoshi Nakamizo, Sachiko Ono, Sho Hanakawa, Takaharu Okada, Nobuhiro Kusuba, Atsushi Otsuka, Akihiko Kitoh, Tetsuya Honda and 14 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
19.5field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 227 citations in OpenAlex.

  1. Article
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  8. T-cell mechanisms in atopic dermatitis.Allergologie select · 2026
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. A single-cell spatial transcriptomic census of human skin anatomy.bioRxiv : the preprint server for biology · 2025
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. CD4Frontiers in immunology · 2025
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 10 institutions in 3 countries.

Yohei Natsuaki1] Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. [2] Department of Dermatology, Kurume University School of Medicine, Fukuoka, Japan.
Gyohei EgawaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Satoshi NakamizoDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Sachiko OnoDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Sho HanakawaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takaharu OkadaResearch Unit for Immunodynamics, RIKEN Research Center for Allergy and Immunology, Kanagawa, Japan.
Nobuhiro KusubaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Atsushi OtsukaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Akihiko KitohDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Tetsuya HondaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Saeko NakajimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Soken TsuchiyaDepartment of Pharmaceutical Biochemistry, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Yukihiko SugimotoDepartment of Pharmaceutical Biochemistry, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Ken J Ishii1] Laboratory of Adjuvant Innovation, National Institute of Biomedical Innovation, Osaka, Japan. [2] Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Hiroko TsutsuiDepartment of Microbiology, Hyogo College of Medicine, Hyogo, Japan.
Hideo YagitaDepartment of Immunology, Juntendo University School of Medicine, Tokyo, Japan.
Yoichiro Iwakura1] Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba, Japan. [2] Medical Mycology Research Center, Chiba University, Chiba, Japan.
Masato Kubo1] Laboratory for Cytokine Regulation, RIKEN center for Integrative Medical Science, Kanagawa, Japan. [2] Division of Molecular Pathology, Research Institute for Biomedical Science, Tokyo University of Science, Chiba, Japan.
Lai guan NgSingapore Immunology Network, Agency for Science, Technology and Research, Biopolis, Singapore.
Takashi HashimotoDepartment of Dermatology, Kurume University School of Medicine, Fukuoka, Japan.
Judilyn FuentesDepartment of Dermatology, Icahn School of Medicine at Mount Sinai School Medical Center, New York, New York,.
Emma Guttman-YasskyDepartment of Dermatology, Icahn School of Medicine at Mount Sinai School Medical Center, New York, New York,.
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 · JPIcahn School of Medicine at Mount Sinai · USKumamoto University · JPRIKEN Center for Integrative Medical Sciences · JPAgency for Science, Technology and Research · SGHyogo Medical University · JPJuntendo University · JPKurume University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It remains largely unclear how antigen-presenting cells (APCs) encounter effector or memory T cells efficiently in the periphery. Here we used a mouse contact hypersensitivity (CHS) model to show that upon epicutaneous antigen challenge, dendritic cells (DCs) formed clusters with effector T cells in dermal perivascular areas to promote in situ proliferation and activation of skin T cells in a manner dependent on antigen and the integrin LFA-1. We found that DCs accumulated in perivascular areas and that DC clustering was abrogated by depletion of macrophages. Treatment with interleukin 1α (IL-1α) induced production of the chemokine CXCL2 by dermal macrophages, and DC clustering was suppressed by blockade of either the receptor for IL-1 (IL-1R) or the receptor for CXCL2 (CXCR2). Our findings suggest that the dermal leukocyte cluster is an essential structure for elicitating acquired cutaneous immunity.

Indexed as

AnimalsCD11c AntigenCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell ProliferationChemokine CXCL2Dendritic CellsDermatitis, ContactFemaleImmunologic MemoryInterleukin-1alphaLymphocyte ActivationLymphocyte Function-Associated Antigen-1MacrophagesMiceMice, Inbred C57BLCD11c AntigenChemokine CXCL2Cxcl2 protein, mouseInterleukin-1alphaLymphocyte Function-Associated Antigen-1Receptors, Interleukin-1Receptors, Interleukin-8B

Identifiers

PMID25240383
OpenAlexW2098276335

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.