Epidermal melanocyte loss in vitiligo, triggered by stresses ranging
from trauma to emo-tional stress, chemical exposure or metabolite
imbalance, to the unknown, can stimulate oxidative stress in pigment
cells which secrete damage-associated molecular patterns that then
initiate innate immune responses. Antigen presentation to melanocytes
leads to stim-ulation of autoreactive T cell responses, with further
targeting of pigment cell. Studies show a pathogenic basis for cellular
stress, innate immune responses and adaptive immun-ity in vitiligo.
Improved understanding of the aetiological mechanisms in vitiligo has
already resulted in successful use of the Jak-1 inhibitors in vitiligo.
In this review we outline the cur-rent understanding of the pathological
mechanisms in vitiligo, and locate loci to which therapeutic attack
might be directed.