Evidence map›Paper›PMID 41345471›Full record

ReviewNature reviews. Disease primers2025

Vitiligo.

Julien Seneschal, Jung Min Bae, Khaled Ezzedine, Iltefat Hamzavi, John E Harris, Barbara Bellei, Davinder Parsad, Thierry Passeron, Nanja van Geel, Katia Boniface and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Disease primers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Lactate Enhances CD8International journal of molecular sciences · 2026
    Article
  12. Review
  13. A pragmatic roadmap toward personalized vitiligo care.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

11 authors.

Julien SeneschalUniversity of Bordeaux, CNRS, Immuno ConcEpT, UMR 5164, Bordeaux, France. julien.seneschal@chu-bordeaux.fr.ORCID http://orcid.org/0000-0003-1139-0908
Jung Min BaeDepartment of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Khaled EzzedineHenri Mondor University Hospital and Epidemiology in Dermatology and Evaluation of Therapeutics (EpiDermE), IMRB - Paris-Est Créteil University, INSERM U955, Créteil, France.
Iltefat HamzaviDepartment of Dermatology, Henry Ford Health, Detroit, MI, USA.
John E HarrisDepartment of Dermatology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID http://orcid.org/0000-0002-7815-6430
Barbara BelleiLaboratory of Cutaneous Physiopathology and Integrated Center of Metabolomics Research, San Gallicano Dermatological Institute, IRCCS, Rome, Italy.
Davinder ParsadDepartment of Dermatology, Venereology & Leprology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Thierry PasseronCentre Hospitalier Universitaire de Nice, Université Côte d'Azur, Nice, France.
Nanja van GeelDepartment of Dermatology, Ghent University Hospital, Ghent, Belgium.
Katia BonifaceUniversity of Bordeaux, CNRS, Immuno ConcEpT, UMR 5164, Bordeaux, France.ORCID http://orcid.org/0000-0003-4428-1222
Mauro PicardoInstituto Dermopatico dell'Immacolata, IRCCS, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitiligo is an acquired autoimmune depigmenting disorder that affects approximately 0.36% of the global population and presents in three forms based on lesion distribution: non-segmental, segmental and mixed vitiligo. Beyond its visible impact on the skin, vitiligo deeply affects mental well-being and quality of life. The pathogenesis of non-segmental vitiligo is influenced by genetic polymorphisms that are linked to immune response and melanogenesis pathways, whereas environmental factors contribute to disease onset. Diagnosis is generally clinical, with laboratory tests or biopsies rarely required. Melanocyte loss involves mechanisms, such as cellular stress, innate immune activation and adaptive immune responses, that specifically target melanocytes, with a central role for tissue-resident memory T cells. This cascade ultimately leads to the depletion of epidermal melanocytes and impairs melanocyte stem cell regeneration. Clinical management emphasizes shared decision-making with three primary objectives: halting depigmentation, initiating repigmentation and sustaining pigment restoration. Signs of active disease help clinicians to identify patients in need of intervention. Treatments approved in the past 2 years offer potential for reversing disease progression, and emerging therapies targeting key pathways to modulate immune activation and stimulate melanocyte regeneration and differentiation are being tested in clinical trials.

Indexed as

VitiligoDisease ProgressionEpidermisHumansMelanocytesMelanogenesisMemory T CellsPhototherapyPolymorphism, GeneticQuality of LifeSkin PigmentationStem Cells

Identifiers

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.