Vitiligo is a chronic skin disorder, affecting 0.5–1% of general population. It is
characterized by skin depigmentation, which can be progressive, resulting from autoimmunity
against the melanocytes and increased susceptibility of melanocytes to oxidative stress.
There are two broad types of vitiligo: segmental vitiligo (SV) and non-segmental vitiligo
(NSV). NSV accounts for roughly 90% of total vitiligo cases [
[1]
]. Autoimmunity is the major hypothesis to explain NSV etiology. Results from recent
genome-wide association studies (GWAS) identified NSV susceptibility genes, which
further supported the hypothesis of NSV as a primary autoimmune disease [
[2]
]. We and other groups recently reported the number and functional defects in peripheral
blood invariant natural killer T (iNKT) cells, or regulatory T lymphocytes, in patients with NSV, which further supports
the theory that NSV is indeed an autoimmune disease [
3
,
4
].Keywords
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Article info
Publication history
Published online: July 18, 2013
Accepted:
April 26,
2013
Identification
Copyright
© 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
