Evidence map›Paper›PMID 32369451›Full record

ArticleJCI insight2020

Type-1 cytokines regulate MMP-9 production and E-cadherin disruption to promote melanocyte loss in vitiligo.

Nesrine Boukhedouni, Christina Martins, Anne-Sophie Darrigade, Claire Drullion, Jérôme Rambert, Christine Barrault, Julien Garnier, Clément Jacquemin, Denis Thiolat, Fabienne Lucchese and 6 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05917561 (Efficacy and Tolerance of the Association of ANIFROLUMAB), which is not on this map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 5% 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.

NCT05917561 phase2unknown statusnot on this mapstarted 2023, after this paper: background citation

Efficacy and Tolerance of the Association of ANIFROLUMAB (300mg) IV Every Four Weeks and Phototherapy Versus Phototherapy in Adults With Progressive Vitiligo: a Randomized Double Blind Prospective, Non Comparative Proof of Concept Phase II Study

TypeinterventionalSponsorUniversity Hospital, BordeauxRan2023 to 2026Enrolled48ConditionsVitiligoArmsAnifrolumab Infusion Product, Placebo
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. The immunology of vitiligo.Nature reviews. Immunology · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Regenerative biomaterials · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Vitiligo.Nature reviews. Disease primers · 2025
    Review
  20. Review
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

16 authors at 4 institutions in 1 country.

Nesrine BoukhedouniINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Christina MartinsINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Anne-Sophie DarrigadeINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Claire DrullionINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Jérôme RambertAquiDerm, University of Bordeaux, Bordeaux, France.
Christine BarraultBioalternatives, Gençay, France.
Julien GarnierBioalternatives, Gençay, France.
Clément JacqueminINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Denis ThiolatINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Fabienne LuccheseINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Franck MorelLaboratoire Inflammation, Tissus Epithéliaux et Cytokines, University of Poitiers, Poitiers, France.
Khaled EzzedineDepartment of Dermatology, Assistance Publique-Hôpitaux de Paris, Hôpital Henri-Mondor, Créteil, France.
Alain TaiebDepartment of Dermatology and Pediatric Dermatology and National Reference Center for Rare Skin Disorders, Hôpital Saint-André, Bordeaux, France.
François-Xavier BernardBioalternatives, Gençay, France.
Julien SeneschalINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Katia BonifaceINSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers (BMGIC), Immunodermatology ATIP-AVENIR, University of Bordeaux, FHU ACRONIM, Bordeaux, France.
Université de Bordeaux · FRHôpital Saint-André · FRHôpitaux Universitaires Henri-Mondor · FRUniversité de Poitiers · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of melanocytes is the pathological hallmark of vitiligo, a chronic inflammatory skin depigmenting disorder induced by exaggerated immune response, including autoreactive CD8 T cells producing high levels of type 1 cytokines. However, the interplay between this inflammatory response and melanocyte disappearance remains to be fully characterized. Here, we demonstrate that vitiligo skin contains a significant proportion of suprabasal melanocytes, associated with disruption of E-cadherin expression, a major protein involved in melanocyte adhesion. This phenomenon is also observed in lesional psoriatic skin. Importantly, apoptotic melanocytes were mainly observed once cells were detached from the basal layer of the epidermis, suggesting that additional mechanism(s) could be involved in melanocyte loss. The type 1 cytokines IFN-γ and TNF-α induce melanocyte detachment through E-cadherin disruption and the release of its soluble form, partly due to MMP-9. The levels of MMP-9 are increased in the skin and sera of patients with vitiligo, and MMP-9 is produced by keratinocytes in response to IFN-γ and TNF-α. Inhibition of MMP-9 or the JAK/STAT signaling pathway prevents melanocyte detachment in vitro and in vivo. Therefore, stabilization of melanocytes in the basal layer of the epidermis by preventing E-cadherin disruption appears promising for the prevention of depigmentation occurring in vitiligo and during chronic skin inflammation.

Indexed as

MAP Kinase Signaling SystemAnimalsCadherinsHumansInterferon-gammaKeratinocytesMatrix Metalloproteinase 9MelanocytesMiceTumor Necrosis Factor-alphaVitiligoCadherinsCdh1 protein, mouseIFNG protein, humanIFNG protein, mouseInterferon-gammaMatrix Metalloproteinase 9MMP9 protein, humanMmp9 protein, mouseTumor Necrosis Factor-alphaAutoimmune diseasesCytokinesDermatologyInflammationSkin

Identifiers

PMID32369451
PMCPMC7308056
OpenAlexW3022441811

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.