Engineering a new mouse model for vitiligo.
Although the precise mechanisms that trigger vitiligo remain elusive, autoimmune responses mediate its progression. The development of therapies has been impeded by a paucity of animal models, since mice lack interfollicular melanocytes, the primary targets in vitiligo. In this issue, Harris et al. describe a mouse model in which interfollicular melanocytes are retained by Kit ligand overexpression and an immune response is initiated by transplanting melanocyte-targeting CD8+ T cells.
The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA.
Prashiela
P
Manga
Seth J
SJ
Orlow
D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology*; D006801:Humans; D007371:Interferon-gamma / Q000502:physiology*; D012867:Skin / Q000276:immunology*; D014820:Vitiligo / Q000276:immunology*
D007371:Interferon-gamma