Enhanced bleaching treatment: Opportunities for immune-assisted melanocyte suicide in vitiligo

Kirsten C. Webb, Jonathan M. Eby, Vidhya Hariharan, Claudia Hernandez, Rosalie M. Luiten, I. Caroline Le Poole*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Depigmentation in vitiligo occurs by progressive loss of melanocytes from the basal layer of the skin, and can be psychologically devastating to patients. T cell-mediated autoimmunity explains the progressive nature of this disease. Rather than being confronted with periods of rapid depigmentation and bouts of repigmentation, patients with long-standing, treatment-resistant vitiligo can undergo depigmentation treatment. The objective is to remove residual pigmentation to achieve a cosmetically acceptable result - that of skin with a uniform appearance. In the United States, only the use of mono-benzyl ether of hydroquinone (MBEH) is approved for this purpose. However, satisfactory results can take time to appear, and there is a risk of repigmentation. MBEH induces necrotic melanocyte death followed by a cytotoxic T-cell response to remaining, distant melanocytes. As cytotoxic T-cell responses are instrumental to depigmentation, we propose that combining MBEH with immune adjuvant therapies will accelerate immune-mediated melanocyte destruction to achieve faster, more definitive depigmentation than with MBEH alone. As Toll-like Receptor (TLR) agonists - imiquimod, CpG, and Heat Shock Protein 70 (HSP 70) - all support powerful Th1 responses, we propose that using MBEH in combination with these agents can achieve superior depigmentation results for vitiligo patients.

Original languageEnglish (US)
Pages (from-to)529-533
Number of pages5
JournalExperimental Dermatology
Issue number8
StatePublished - Aug 2014


  • Bleaching phenols
  • CpG
  • HSP70
  • Imiquimod
  • Monobenzone
  • T cells
  • Vitiligo

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology


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