Vitiligo is an autoimmune condition for which the development of effective therapeutic interventions has proved challenging. Research into the pathogenesis of this condition has led to the identification of therapeutic targets and promising new and emerging treatments. Combination therapies including light exposure have also demonstrated efficacy. Research in mouse models have been effective as gene expression is similar in both mouse and human vitiligo. Research findings for vitiligo may have broader applicability for similar organ-specific autoimmune conditions.

• Vitiligo affects 3.25 million individuals in the US and 74 million individuals worldwide.
• Onset is before the age of 20 years in 50% of patients.
• Vitiligo is associated with diseases such as Type 1 diabetes, lupus, Hashimoto thyroiditis, pernicious anemia, and Addison’s disease.

An increased understanding of the pathogenesis of vitiligo can facilitate development of effective therapies.

• T cells kill melanocytes, and perilesional cytotoxic T cells demonstrate ability to eradicate pigment cells; this understanding is effective in treating vitiligo. T cells can effectively mediate targeted autoimmune tissue destruction [1].
• Gene expression demonstrates similarities in mouse and human vitiligo. Research in mouse models demonstrates that neutralizing the interferon (IFN)-γ prevents autoreactive CD8+ T-cell accumulation and depigmentation, could therefore be a promising approach to new therapies [2].
• The chemokine CXCL 10 is elevated in vitiligo patients. CXCL 10 inhibition has been identified as a therapeutic target and has resulted in disease reversal and repigmentation in mice [3].
• Targeting CXCR3 can prevent and reverse vitiligo in mice, however, further study is warranted [4].
• Keratinocyte-derived chemokines may serve as biomarkers of vitiligo and targeting IFN-γ signaling in keratinocytes could be effective in the development of topical therapies [5].

• Tofacitinib citrate is an oral JAK inhibitor that has demonstrated significant repigmentation in vitiligo patients [6].
• Studies indicate that JAK inhibitor tofacitinib may require concomitant light exposure for efficacy in repigmentation in vitiligo patients. Low light may be sufficient, as contrasted with phototherapy. The role of light exposure is the apparent stimulation of melanocyte regeneration, whereas JAK inhibitors suppress T cell mediators [7].
• Oral ruxolitinib has been associated with rapid repigmentation in one case study when administered for alopecia areata in a vitiligo patient with both conditions [8].
• Topical ruxolitinib, a JAK inhibitor, has demonstrated efficacy in the treatment of vitiligo. The efficacy of topical ruxolitinib 1.5 % cream administered twice daily over 20 weeks was established in a recent study, with the primary outcome measure evaluated being a change from baseline in Vitiligo Area Scoring (VAS) Index. Patients using this topical therapy experienced significant facial repigmentation [9].