Asebia-2J (Scd1ab2J): A New Allele and a Model for Scarring Alopecia

摘要: A spontaneous, autosomal, recessive mouse mutation exhibiting mild scaly skin, progressive scarring alopecia, slightly runted growth, and photophobia arose at The Jackson Laboratory in 1993 the inbred strain DBA/1LacJ. Because this mutant showed genetic, anatomical, laboratory similarities to asebia mutation, crosses were done between new mice carrying asebia-J allele. F1 offspring affected, indicating two mutants allelic, was named asebia-2J. Careful histological analysis of skin development homozygous heterozygous for either or asebia-2J revealed that both types are very similar regardless their background. Notable histopathological features allele included extreme sebaceous gland hypoplasia, abnormally long anagen follicles, retained inner root sheath, hair fiber perforation follicle base, follicular replacement by scarring. In article we present a pathogenetic hypothesis based on importance sheath dissociation: absence functional is destroyed. cutaneous pathology underscores biology presents an animal model studying human alopecias, which characteristically begin with ablation.