A review and a new hypothesis for non-immunological pathogenetic mechanisms in vitiligo

Research output: Contribution to journalArticle

112 Citations (Scopus)

Abstract

Vitiligo is an acquired depigmenting disorder characterized by the loss of functioning epidermal melanocytes because of multifactorial and overlapping pathogenetic mechanisms. Besides the immunological approach, the study of the metabolic deregulations leading to toxic damage of the melanocytes appears to be more and more relevant. It was only last year that the first in vitro evidence supporting the link and the temporal sequence between the immune response and the cellular oxidative stress was provided, suggesting that the intrinsic damage of the melanocytes is primitive. What can be the guide line of the multiple altered metabolisms? A compromised membrane could render the cell sensitive to the external and internal agents differently, usually ineffective on the cell activity and survival. The primitive altered arrangement of the lipids may affect the transmembrane housing of proteins with enzymatic or receptorial activities, also conferring on them antigenic properties.

Original languageEnglish
Pages (from-to)406-411
Number of pages6
JournalPigment Cell Research
Volume19
Issue number5
DOIs
Publication statusPublished - Oct 2006

Fingerprint

Vitiligo
Oxidative stress
Deregulation
melanocytes
Poisons
Melanocytes
Metabolism
Membranes
Lipids
Proteins
metabolic studies
Cellular Immunity
Cell Survival
Oxidative Stress
oxidative stress
immune response
cells
metabolism
lipids
proteins

Keywords

  • Intrinsic melanocyte damage
  • Melanocyte loss
  • Membrane impairment
  • Vitiligo

ASJC Scopus subject areas

  • Cell Biology
  • Agronomy and Crop Science
  • Plant Science
  • Clinical Biochemistry
  • Developmental Biology

Cite this

A review and a new hypothesis for non-immunological pathogenetic mechanisms in vitiligo. / Dell'Anna, Maria Lucia; Picardo, Mauro.

In: Pigment Cell Research, Vol. 19, No. 5, 10.2006, p. 406-411.

Research output: Contribution to journalArticle

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