Monobenzone‐induced depigmentation: from enzymatic blockade to autoimmunity

  title={Monobenzone‐induced depigmentation: from enzymatic blockade to autoimmunity},
  author={Jasper G. van den Boorn and Cornelis J. M. Melief and Rosalie M. Luiten},
  journal={Pigment Cell \& Melanoma Research},
Autoimmune side‐effects such as vitiligo regularly occur during melanoma immunotherapy. As vitiligo development is associated with a superior prognosis, the active induction of vitiligo in melanoma patients can be a useful tactic. The potent skin‐depigmenting agent monobenzone can be used successfully for this purpose. However, until recently, the mechanism of action behind monobenzone‐induced skin depigmentation was unclear. Lately, the mechanistic basis for the augmented immunogenicity of… 

A mouse model of vitiligo induced by monobenzone

It is demonstrated that monobenzone‐induced skin depigmentation on the non‐exposed sites and that the severity of lesions depended on drug dosage, which suggests good potential of the mouse model for use in vitiligo research.

Mouse Model for Human Vitiligo

The first mouse model of vitiligo that develops epidermal depigmentation, similar to disease in human patients is discussed, and how to use this model to inform clinical studies is described.

The Role of NKG2D in Vitiligo

This review examines how melanocyte stress leads to the expression of ligands that are recognized by the activating receptor NKG2D, and how its signaling results in the turning of T cells against self (melanocyte suicide by proxy).

Simvastatin prevents and reverses depigmentation in a mouse model of vitiligo

It is found that simvastatin both prevented and reversed depigmentation in the mouse model of vitiligo, and reduced the number of infiltrating autoreactive CD8+ T cells in the skin.

Mechanism of action of 4‐substituted phenols to induce vitiligo and antimelanoma immunity

It is concluded that 4‐substituted phenols can induce specific T‐cell responses against melanocytes and melanoma cells, also acting at distant, unexposed body sites, and may confer a risk of chemical vitiligo.

Vitiligo: How do oxidative stress-induced autoantigens trigger autoimmunity?

The Evaluation of Vitiligous lesions Repigmentation after the Administration of Atorvastatin calcium salt and Simvastatin-acid sodium salt in patients with active vitiligo (EVRAAS), a pilot study: study protocol for a randomized controlled trial

This study is the first to evaluate safety and efficacy of the topical use of statins in patients presenting with nonsegmental vitiligo (NSV), and it is shown that statins act through several immunological pathways, potentially reversing undesirable phenomena underlying autoimmune Vitiligo pathogenesis.

The convergence theory for vitiligo: A reappraisal

The convergence theory continues to provide a comprehensive viewpoint of vitiligo aetiology and serves to intertwine aetiologic pathways and will help to define pathways amenable to disease intervention in individual patients.

Depigmentation Therapies for Vitiligo.



Skin-depigmenting agent monobenzone induces potent T-cell autoimmunity toward pigmented cells by tyrosinase haptenation and melanosome autophagy.

The previously unknown mechanism of inducing robust anti-melanoma immunity by the vitiligo-inducing compound monobenzone is reported and represents a promising and readily applicable compound for immunotherapy in melanoma patients.

[Acquired leukomelanoderma caused by topical depigmenting agents].

Adverse effects were observed--irritation and local sensitization--depigmentation locally and at a distance from the treated areas--melanoleukodermia among asiatics--no repigmentation: therefore treatment with MBEH has been used by Mosher in extensive vitiligo on the unaffected areas.

Vitiligo pathogenesis: autoimmune disease, genetic defect, excessive reactive oxygen species, calcium imbalance, or what else?

As a more effective therapy for this common, often disfiguring pigmentary disorder is direly needed, it must strive harder to settle the pathogenesis debate definitively – on the basis of sound experimental evidence, rather than by a war of dogmatic theories.

Contact hypersensitivity to monobenzyl ether of hydroquinone used to treat vitiligo

A 37-year-old man presented with patches of erythema and vesiculation on the forearms and dorsa of the hands that appeared 2 days after working on an aquarium without gloves, and was tested with a standard series and was positive to Disperse Blue.

Effective Melanoma Immunotherapy in Mice by the Skin-Depigmenting Agent Monobenzone and the Adjuvants Imiquimod and CpG

MIC therapy is effective in eradicating melanoma, by vigilantly incorporating NK-, B- and T cells in its therapeutic effect.

On the etiology of contact/occupational vitiligo.

The data suggests that tyrosinase-related protein-1, rather than tyOSinase, facilitates toxicity, possibly by catalytic conversion of the compounds, which results in the generation of radical oxygen species.

Immunoregulatory mechanisms involved in elicitation of allergic contact hypersensitivity.

Hypopigmenting agents: an updated review on biological, chemical and clinical aspects.

An overview of agents causing hypopigmentation in human skin is presented and it is suggested that Mammalian skin or at least keratinocytes/melanocytes co-cultures should be preferred rather than pure melanocyte cultures or soluble tyrosinase.

Mechanism of depigmentation by hydroquinone.

Findings indicate that HQ affects not only the formation, melanization, and degradation of melanosomes, but that it affects also the membraneous structures of melanocytes and eventually causes necrosis of whole melanocytes.

Evaluation of monobenzone.

A multitude of diseases will produce areas of increased pigmentation in the skin, often a cosmetic liability, and long-term clinical studies have demonstrated that it will not produce uniform, controllable depigmentation.