Evidence map›Paper›PMID 37275386›Full record

ReviewFrontiers in medicine2023

Melanocyte-keratinocyte cross-talk in vitiligo.

Ahmed Ahmed Touni, Rohan S Shivde, Harika Echuri, Rasha T A Abdel-Aziz, Hossam Abdel-Wahab, Roopal V Kundu, I Caroline Le Poole

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  9. Review
  10. Article
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  13. Review
  14. Article
  15. Article
  16. Article
  17. The Anti-Vitiligo Effects of Feshurin In Vitro fromPharmaceuticals (Basel, Switzerland) · 2024
    Article
  18. Review
  19. Article
  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

7 authors at 3 institutions in 2 countries.

Ahmed Ahmed TouniDepartment of Dermatology, Faculty of Medicine, Minia University, Minia, Egypt.
Rohan S ShivdeDepartment of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Harika EchuriDepartment of Dermatology, Emory University, Atlanta, GA, United States.
Rasha T A Abdel-AzizDepartment of Dermatology, Faculty of Medicine, Minia University, Minia, Egypt.
Hossam Abdel-WahabDepartment of Dermatology, Faculty of Medicine, Minia University, Minia, Egypt.
Roopal V KunduDepartment of Dermatology, Faculty of Medicine, Minia University, Minia, Egypt.
I Caroline Le PooleDepartment of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Minia University · EGNorthwestern University · USEmory University · US

Funding

Northwestern University Skin Disease Research Center Resource-based CenterP30AR075049 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Amy S Paller · 2019 to 2026
$6.6M
NIAMS NIH HHS P30 AR075049
6 · The paper itself

Abstract

Vitiligo is a common acquired pigmentary disorder that presents as progressive loss of melanocytes from the skin. Epidermal melanocytes and keratinocytes are in close proximity to each other, forming a functional and structural unit where keratinocytes play a pivotal role in supporting melanocyte homeostasis and melanogenesis. This intimate relationship suggests that keratinocytes might contribute to ongoing melanocyte loss and subsequent depigmentation. In fact, keratinocyte dysfunction is a documented phenomenon in vitiligo. Keratinocyte apoptosis can deprive melanocytes from growth factors including stem cell factor (SCF) and other melanogenic stimulating factors which are essential for melanocyte function. Additionally, keratinocytes control the mobility/stability phases of melanocytes via matrix metalloproteinases and basement membrane remodeling. Hence keratinocyte dysfunction may be implicated in detachment of melanocytes from the basement membrane and subsequent loss from the epidermis, also potentially interfering with repigmentation in patients with stable disease. Furthermore, keratinocytes contribute to the autoimmune insult in vitiligo. Keratinocytes express MHC II in perilesional skin and may present melanosomal antigens in the context of MHC class II after the pigmented organelles have been transferred from melanocytes. Moreover, keratinocytes secrete cytokines and chemokines including CXCL-9, CXCL-10, and IL-15 that amplify the inflammatory circuit within vitiligo skin and recruit melanocyte-specific, skin-resident memory T cells. In summary, keratinocytes can influence vitiligo development by a combination of failing to produce survival factors, limiting melanocyte adhesion in lesional skin, presenting melanocyte antigens and enhancing the recruitment of pathogenic T cells.

Indexed as

adhesionantigen presentationapoptosischemokinesgrowth factorsmelanosome transferstressvitiligo

Identifiers

PMID37275386
PMCPMC10235633
OpenAlexW4377139482

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.