Evidence map›Paper›PMID 33516870›Full record

ArticleThe Journal of allergy and clinical immunology2021

Skin-resident natural killer T cells participate in cutaneous allergic inflammation in atopic dermatitis.

ZhengWang Sun, Ji Hye Kim, Seo Hyeong Kim, Hye Ran Kim, KeLun Zhang, Youdong Pan, Min Kyung Ko, Bo Mi Kim, Howard Chu, Hee Ra Lee and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Weak Sensitizers May Be Associated with CD80 Polymorphisms: Implications for Systemic Contact Dermatitis.JID innovations : skin science from molecules to population health · 2025
    Article
  7. Cutaneous T cell immunity.Nature immunology · 2025
    Review
  8. Article
  9. Article
  10. CD2 expressing innate lymphoid and T cells are critical effectors of immunopathogenesis in hidradenitis suppurativa.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Role of fibroblasts in nonfibrotic autoimmune skin diseases.Molecular medicine (Cambridge, Mass.) · 2024
    Review
  13. Article
  14. Article
  15. Tissue-Resident Memory T Cells in Allergy.Clinical reviews in allergy & immunology · 2024
    Review
  16. Review
  17. Novel insights into atopic dermatitis.The Journal of allergy and clinical immunology · 2023
    Review
  18. Review
  19. Article
  20. Atopic Dermatitis Is Associated with Preeclampsia and Endometriosis.JID innovations : skin science from molecules to population health · 2022
    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

23 authors at 5 institutions in 2 countries.

ZhengWang SunDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Ji Hye KimDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 Project, Graduate School of Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Seo Hyeong KimDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 Project, Graduate School of Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Hye Ran KimDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
KeLun ZhangDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 Project, Graduate School of Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Youdong PanDepartment of Dermatology and Harvard Skin Disease Research Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Min Kyung KoDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Bo Mi KimDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Howard ChuDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Hee Ra LeeDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Hye Li KimDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 Project, Graduate School of Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Ji Hyung KimDivision of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Korea.
Xiujun FuCenter for Systems Biology and Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.
Young-Min HyunBrain Korea 21 Project, Graduate School of Medical Science, Yonsei University College of Medicine, Seoul, Korea; Department of Anatomy, Yonsei University College of Medicine, Seoul, Korea.
Ki Na YunBiomedical Omics Group, Korea Basic Science Institute, Ochang, Korea.
Jin Young KimBiomedical Omics Group, Korea Basic Science Institute, Ochang, Korea.
Dong Won LeeDepartment of Plastic and Reconstructive Surgery, Institute for Human Tissue Restoration, Yonsei University College of Medicine, Seoul, Korea.
Seung Yong SongDepartment of Plastic and Reconstructive Surgery, Institute for Human Tissue Restoration, Yonsei University College of Medicine, Seoul, Korea.
Charles P LinCenter for Systems Biology and Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.
Rachael A ClarkDepartment of Dermatology and Harvard Skin Disease Research Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Kwang Hoon LeeDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 Project, Graduate School of Medical Science, Yonsei University College of Medicine, Seoul, Korea. Electronic address: kwanglee@yuhs.ac.
Thomas S KupperDepartment of Dermatology and Harvard Skin Disease Research Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass. Electronic address: tkupper@bwh.harvard.edu.
Chang Ook ParkDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 Project, Graduate School of Medical Science, Yonsei University College of Medicine, Seoul, Korea; Department of Dermatology and Harvard Skin Disease Research Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass. Electronic address: copark@yuhs.ac.
Yonsei University · KRKorea Basic Science Institute · KRHarvard University · USBrigham and Women's Hospital · USCenter for Systems Biology · US

Funding

Skin Homing T CellsR01AR065807 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI KUPPER, THOMAS S. · 2013 to 2022
$6.3M
Vaccination to generate protective tissue resident T cellsR01AI097128 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI CLARK, RACHAEL ANN, KUPPER, THOMAS S. · 2011 to 2015
$6.1M
Generation of Robust Resident Memory T cells in Barrier Tissues through Skin VaccinationR01AI127654 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI CLARK, RACHAEL ANN, KUPPER, THOMAS S. · 2017 to 2021
$6.0M
SKIN HOMING T CELLS--MOLECULAR CHARACTERIZATION OF CLAR01AI041707 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KUPPER, THOMAS S. · 1997 to 2012
$4.1M
CTCL immunobiology: lessons from alemtuzumabR01AR063962 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI CLARK, RACHAEL ANN · 2013 to 2017
$1.8M
NIAID NIH HHS R01 AI041707NIAID NIH HHS R01 AI097128NIAID NIH HHS R01 AI127654NIAMS NIH HHS R01 AR063962NIAMS NIH HHS R01 AR065807
6 · The paper itself

Abstract

backgroundNatural killer T (NKT) cells are unconventional T cells that bridge innate and adaptive immunity. NKT cells have been implicated in the development of atopic dermatitis (AD).

objectiveWe aimed to investigate the role of NKT cells in AD development, especially in skin.

methodsGlobal proteomic and transcriptomic analyses were performed by using skin and blood from human healthy-controls and patients with AD. Levels of CXCR4 and CXCL12 expression in skin NKT cells were analyzed in human AD and mouse AD models. By using parabiosis and intravital imaging, the role of skin CXCR4

resultsCXCR4 and its cognate ligand CXCL12 were significantly upregulated in the skin of humans with AD by global transcriptomic and proteomic analyses. CXCR4

conclusionsCXCR4

Indexed as

AnimalsChemokine CXCL12Dermatitis, AtopicFemaleGene Expression ProfilingHumansMiceNatural Killer T-CellsProteomicsReceptors, CXCR4SkinChemokine CXCL12Receptors, CXCR4Atopic dermatitisCXCL12CXCR4natural killer T cellsthymic stromal lymphopoietintissue-resident memory T cellsT(RM) cells

Identifiers

PMID33516870
PMCPMC9272812
OpenAlexW3122027428

What OpenQuestion holds

Textmetadata
LicenceTDM
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.