Role of Cytokines in Vitiligo: Pathogenesis and Possible Targets for Old and New Treatments

Int J Mol Sci. 2021 Oct 22;22(21):11429. doi: 10.3390/ijms222111429.

Abstract

Vitiligo is a chronic autoimmune dermatosis of which the pathogenesis remains scarcely known. A wide variety of clinical studies have been proposed to investigate the immune mediators which have shown the most recurrency. However, such trials have produced controversial results. The aim of this review is to summarize the main factors involved in the pathogenesis of vitiligo, the latest findings regarding the cytokines involved and to evaluate the treatments based on the use of biological drugs in order to stop disease progression and achieve repigmentation. According to the results, the most recurrent studies dealt with inhibitors of IFN-gamma and TNF-alpha. It is possible that, given the great deal of cytokines involved in the lesion formation process of vitiligo, other biologics could be developed in the future to be used as adjuvants and/or to entirely replace the treatments that have proven to be unsatisfactory so far.

Keywords: autoimmune diseases; biological drugs; biologics; depigmentation; dermatoses; inflammation; interleukins; oxidative stress; skin; vitiligo.

Publication types

  • Review

MeSH terms

  • Autoimmune Diseases / drug therapy
  • Autoimmune Diseases / pathology*
  • Biological Products / therapeutic use*
  • Cytokines / metabolism*
  • Exonucleases / genetics
  • HLA-DQ beta-Chains / genetics
  • HLA-DRB1 Chains / genetics
  • Humans
  • Interferon-gamma / antagonists & inhibitors
  • Keratinocytes / metabolism
  • Melanocytes / pathology
  • Pigmentation / physiology
  • Skin / pathology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Vitiligo / drug therapy*
  • Vitiligo / pathology*

Substances

  • Biological Products
  • Cytokines
  • HLA-DQ beta-Chains
  • HLA-DQB1 antigen
  • HLA-DRB1 Chains
  • HLA-DRB4*01:01 antigen
  • IFNG protein, human
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • Exonucleases
  • MYG1 protein, human