Figure 1.

(A) IFN- γ signaling and the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway in vitiligo. (B) The secretion of MMP-9 by keratinocytes, in response to IFN-γ and TNF-α, induced melanocytes detachment through E-cadherin disruption and released its soluble form, in the vitiligo skin comparing with the normal skin. (C) Illustrates the vitiligo pathogenesis: the IFN-γ-chemokine axis, with its associated positive-feedback loop: the autoreactive CD8+ T cells produce IFN-γ, which promotes depigmentation; IFN-γ simultaneously stimulates keratinocytes to express CXCR3 that binds to CXCL9 to recruit more melanocyte-reactive T cells. In addition, CXCL10 recruits T cells within the skin through the CXCR3 receptor, which prolongs and exacerbates the established vitiligo lesion. (D) The potential target for JAK inhibitors to treat vitiligo.