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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Alopecia areata in aging C3H/HeJ mice.

A disease closely resembling human alopecia areata was found in a large production colony of C3H/HeJ mice that had no evidence of thyroid dysfunction or an infectious etiology. Alopecia developed diffusely or in circular areas on the dorsal surface. Histologically, the changes in this non-scarring alopecia were limited to anagen follicles that were surrounded by mononuclear cells. This infiltrate, composed primarily of cytotoxic (CD8+) and helper (CD4+) T cells, was associated with follicular and hair shaft dystrophy. This infiltrate was markedly reduced by intralesional injection of triamcinolone acetonide with subsequent hair regrowth in the affected site. Pedigree tracing of affected C3H/HeJ mice suggests that this non-scarring alopecia may be an inherited disease. Breeding results of normal haired mice with alopecia areata mice or between alopecia areata mice suggests that this is a complex polygenic disease with a female predominance at younger ages. Female mice developed the disease earlier than male mice (3-5 versus > 6 months), with equal numbers affected by 18 months of age. The relative incidence of alopecia areata in one production colony of C3H/HeJ mice was 0.25% for female and 0.035% for male mice, but selective breeding has raised the frequency to nearly 20%. The frequency in an aging colony selectively bred for inflammatory bowel disease reached 4.7%, with equal sex distribution, for mice over 18 months of age, suggesting that this might be a common aging change in C3H/HeJ mice. This C3H/HeJ mouse disease may prove to be a valuable animal model to study specific subtypes of human alopecia areata.[1]


  1. Alopecia areata in aging C3H/HeJ mice. Sundberg, J.P., Cordy, W.R., King, L.E. J. Invest. Dermatol. (1994) [Pubmed]
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