Hypothesis: Possible role for the melatonin receptor in vitiligo: Discussion paper

A. Slominski, Ralf Paus, A. Bomirski

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

A new unifying hypothesis for the aetiology of vitiligo is proposed, in which we postulate that the final destruction of melanocytes in vitiligo results from a cascade of reactions initiated by a disregulation of melanogenesis, caused by activation of the melatonin receptor. These events result in the high and uncontrolled production of free radicals and toxic products of melanogenesis which sequentially damage or destroy melanocytes and keratinocytes, provoke an autoimmune response against exposed intracellular or altered cell surface antigenes, and increase the propensity of melanocytes to undergo malignant transformation.

Original languageEnglish (US)
Pages (from-to)539-541
Number of pages3
JournalJournal of the Royal Society of Medicine
Volume82
Issue number9
StatePublished - Jan 1 1989
Externally publishedYes

Fingerprint

Melatonin Receptors
Vitiligo
Melanocytes
Poisons
Autoimmunity
Keratinocytes
Free Radicals

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Hypothesis : Possible role for the melatonin receptor in vitiligo: Discussion paper. / Slominski, A.; Paus, Ralf; Bomirski, A.

In: Journal of the Royal Society of Medicine, Vol. 82, No. 9, 01.01.1989, p. 539-541.

Research output: Contribution to journalArticle

@article{bcdf78c737f34ba8b27287cbfd29d6d9,
title = "Hypothesis: Possible role for the melatonin receptor in vitiligo: Discussion paper",
abstract = "A new unifying hypothesis for the aetiology of vitiligo is proposed, in which we postulate that the final destruction of melanocytes in vitiligo results from a cascade of reactions initiated by a disregulation of melanogenesis, caused by activation of the melatonin receptor. These events result in the high and uncontrolled production of free radicals and toxic products of melanogenesis which sequentially damage or destroy melanocytes and keratinocytes, provoke an autoimmune response against exposed intracellular or altered cell surface antigenes, and increase the propensity of melanocytes to undergo malignant transformation.",
author = "A. Slominski and Ralf Paus and A. Bomirski",
year = "1989",
month = "1",
day = "1",
language = "English (US)",
volume = "82",
pages = "539--541",
journal = "Journal of the Royal Society of Medicine",
issn = "0141-0768",
publisher = "SAGE Publications Ltd",
number = "9",

}

TY - JOUR

T1 - Hypothesis

T2 - Possible role for the melatonin receptor in vitiligo: Discussion paper

AU - Slominski, A.

AU - Paus, Ralf

AU - Bomirski, A.

PY - 1989/1/1

Y1 - 1989/1/1

N2 - A new unifying hypothesis for the aetiology of vitiligo is proposed, in which we postulate that the final destruction of melanocytes in vitiligo results from a cascade of reactions initiated by a disregulation of melanogenesis, caused by activation of the melatonin receptor. These events result in the high and uncontrolled production of free radicals and toxic products of melanogenesis which sequentially damage or destroy melanocytes and keratinocytes, provoke an autoimmune response against exposed intracellular or altered cell surface antigenes, and increase the propensity of melanocytes to undergo malignant transformation.

AB - A new unifying hypothesis for the aetiology of vitiligo is proposed, in which we postulate that the final destruction of melanocytes in vitiligo results from a cascade of reactions initiated by a disregulation of melanogenesis, caused by activation of the melatonin receptor. These events result in the high and uncontrolled production of free radicals and toxic products of melanogenesis which sequentially damage or destroy melanocytes and keratinocytes, provoke an autoimmune response against exposed intracellular or altered cell surface antigenes, and increase the propensity of melanocytes to undergo malignant transformation.

UR - http://www.scopus.com/inward/record.url?scp=0024395461&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024395461&partnerID=8YFLogxK

M3 - Article

C2 - 2552111

AN - SCOPUS:0024395461

VL - 82

SP - 539

EP - 541

JO - Journal of the Royal Society of Medicine

JF - Journal of the Royal Society of Medicine

SN - 0141-0768

IS - 9

ER -