Vitiligo Pathogenesis and Emerging Treatments.
The pathogenesis of vitiligo involves interplay between intrinsic and extrinsic melanocyte defects, innate immune inflammation, and T-cell-mediated melanocyte destruction. The goal of treatment is to not only halt disease progression but also promote repigmentation through melanocyte regeneration, proliferation, and migration. Treatment strategies that address all aspects of disease pathogenesis and repigmentation are likely to have greatest efficacy, a strategy that may require combination therapies. Current treatments generally involve nontargeted suppression of autoimmunity, whereas emerging treatments are likely to use a more targeted approach based on in-depth understanding of disease pathogenesis, which may provide higher efficacy with a good safety profile.
Department of Dermatology, University of Massachusetts Medical School, Worcester, MA 01605, USA; Department of Dermatology, Tehran University of Medical Sciences, 415 Taleqani Avenue, Tehran 1416613675, Iran.
Mehdi
M
Rashighi
Department of Dermatology, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: John.Harris@umassmed.edu.
John E
JE
Harris
D056704:Adaptive Immunity / Q000276:immunology; D000975:Antioxidants / Q000627:therapeutic use; D015551:Autoimmunity / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008544:Melanocytes / Q000276:immunology* / Q000378:metabolism; D018384:Oxidative Stress; D010789:Phototherapy; D012038:Regeneration; D017634:Self Tolerance / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014820:Vitiligo / Q000276:immunology* / Q000628:therapy
D000975:Antioxidants; D007166:Immunosuppressive Agents
Autoimmunity; Cellular stress; Chemokines; Melanogenesis; Targeted therapy; Vitiligo