ABSTRACT
Alopecia areata in C3H/HeJ mice appears not to be due to a single-gene mutation, which makes determination of the underlying genetics difficult. Preliminary results of ongoing breeding studies suggest that alopecia areata of aging C3H/HeJ mice is a complex polygenic trait. The alopecia that developed in aging C3H/HeJ mice was found to be due to what appeared to be an autoimmune response to anagen-stage hair follicles. A variety of unrelated background diseases occur in aging C3H/HeJ mice which include cardiac calcinosis, retinal dysplasia, typhilitis, lingual mineralization, blepharitis, preputial gland hyperkeratosis, renal mineralization, Meckel's diverticulum, otitis media, skeletal muscle mineralization, coccygeal hemivertebrae, hepatic telangiectasis, ovarian cysts and tumors, and proctitis. In addition, more than 85% of C3H/HeJ mice over 15 months of age develop hepatocellular adenomas and simple tubular mammary adenocarcinomas. The C3H/HeJ mice with alopecia areata have the same lipopolysaccharide response as those with normal hair coats.
