Interfering with the IFN-γ/CXCL10 pathway to develop new targeted treatments for vitiligo

Mehdi Rashighi, John E. Harris


Vitiligo is a common, disfiguring autoimmune disease caused by the destruction of epidermal melanocytes. It presents with patchy depigmentation of skin, which significantly affects patients’ self-esteem and quality of life. The mainstay of vitiligo treatment is topical steroids, calcineurin inhibitors, and/or narrow band UVB (nbUVB) phototherapy (1). These treatments utilize a non-targeted approach with moderate efficacy, but are used off-label, as they are not Food and Drug Administration (FDA)-approved for use in vitiligo. Currently, the only FDA-approved treatment for the disease is monobenzone cream (Benoquin®), which is actually used to permanently depigment, rather than repigment, the skin. This treatment results in an even skin tone, and can be appropriate for patients with extensive disease (2,3). However, it is one of a limited number of treatments used in medicine to intentionally make disease worse, and treatments focused on reversing vitiligo, with better efficacy, are greatly needed.