vde12002-sup-0001-FigS1.tifimage/tif9712KFigure S1. Welsh pony with pemphigus vulgaris (PV).
vde12002-sup-0002-FigS2.tifimage/tif3547KFigure S2. Welsh pony with PV: oral ulcers.
vde12002-sup-0003-FigS3.tifimage/tif1625KFigure S3. Indirect immunofluorescence showing the presence of circulating antikeratinocyte IgG autoantibodies (equine lip substrate) in a ‘bottom heavy’ pattern (bright green fluorescence – white arrow) compatible with an anti-desmoglein (Dsg)-3 response.
vde12002-sup-0004-FigS4.tifimage/tif18116KFigure S4. Welsh pony with PV, 2 weeks after initiating systemic corticosteroid treatment.
vde12002-sup-0005-FigS5.tifimage/tif7363KFigure S5. Welsh pony with PV, 6 weeks after tapering and finally discontinuing prednisolone dosage due to laminitis.
vde12002-sup-0006-FigS6.tifimage/tif15394KFigure S6. Welsh pony with PV: muzzle at necropsy.
vde12002-sup-0007-FigS7.tifimage/tif4053KFigure S7. Photomicrograph of skin taken at necropsy. Marked suprabasilar clefting and vesicle formation containing serum and hemorrhage and a few free floating acantholytic keratinocytes (arrow pointing up). The base of the vesicle is lined by basal cells (‘tombstones’; arrow pointing down). H & E, bar: 200 mm.
vde12002-sup-0008-FigS8.tifimage/tif9408KFigure S8. Pemphigus vulgaris serum diluted to 1:50 was preincubated with either control supernatants (C) or cDsg3 (D), and then subjected to indirect immunofluorescence using equine buccal mucosa as substrate. The reactivity of IgG against equine keratinocytes (C) was absorbed by cDsg3 (D) (absence of fluorescence). Bar = 100 μm.

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