Summary
Epidermal melanocyte loss in vitiligo, triggered by stresses ranging
from trauma to emotional 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 stimulation of autoreactive T cell responses, with further
targeting of pigment cell. Studies show a pathogenic basis for cellular
stress, innate immune responses and adaptive immunity 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 current understanding of the pathological
mechanisms in vitiligo, and locate loci to which therapeutic attack
might be directed.
Key words: Antibodies, Autoimmunity, Cytokines, Cytotoxic T
Cells, Th1/Th2 Cells