Equine alopecia areata autoantibodies target multiple hair follicle antigens and may alter hair growth. A preliminary study.

Abstract

Several cases of an alopecia areata (AA)-like disease have been reported in mammalian species. How similar this disorder(s) is to human AA is unclear. We have previously shown that human AA is associated with antibodies to hair follicle (HF)-specific antigens and that similar antibody reactivities also occur in the C3H/HeJ "AA" murine model and in dogs with spontaneously occurring AA. The current preliminary study was conducted to determine whether a horse with AA-like hair loss contained circulating antibodies to HE The pathogenic potential of these antibodies was examined by passive transfer into anagen skin of C57BL/ 10 black mice. Indirect immunofluorescence analysis indicated that the equine "AA" serum reacted intensely with the inner root sheath, outer root sheath and pre-cortex of equine HF Immunoblot examination revealed antibodies to a 200-220 kDa doublet and to antigens of 40-60 kDa. Notably, this serum, but not control serum, contained antibodies that selectively immunoprecipitated trichohyalin from HF protein extracts. IgG fractions of serum obtained from an "AA" horse and from a normal control horse were injected into anagen murine skin. Histologically, normal hair regrowth was observed in mice injected with normal equine IgG. By contrast, hair did not re-grow in an area around the injection site of AA-treated mice even 13 weeks after first injection. This skin contained telogen follicles, most often without associated shafts, despite the presence of anagen HF in the remaining dorsum skin. While this study is preliminary, it demonstrates for the first time that antibodies to HF antigens are a feature of AA-like hair loss in horses. Some reactivities (e.g. against trichohyalin) were similar to those previously observed in "AA" dogs. Further, we provide in this pilot study preliminary evidence that such antibodies may disrupt hair re-growth when passively transferred into mice, supporting the view that anti-HF antibodies in AA may have pathogenic potential.