EXPERIMENTAL INDUCTION OF ALOPECIA AREATA-LIKE HAIR LOSS IN C3H HEJ MICE USING FULL-THICKNESS SKIN-GRAFTS/

Alopecia areata (AA)-like hair loss in C3H/HeJ mice provides an excell ent model for human AA disease research. The potential to induce mouse AA in normal haired C3H/HeJ mice at an early age or serially passage the AA phenotype was investigated by exchange of full-thickness skin g rafts. Skin grafts from normal male and female C3H/HeJ, or severe comb ined immunodeficient C3H/SmnC Prkdc(scid)/J, mice onto AA-affected C3H /HeJ mice became inflamed and lost hair (28 of 28), Successful grafts front AA-affected C3H/HeJ mice induced hair loss in histocompatible C3 H/OuJ mice (four of 13) and normal C3H/HeJ mice dependent on age (four of 17 at <31 d and 15 of 15 at >70 d). The AA phenotype was serially transmitted from induced AA mice to normal C3H/HeJ mice (nine of nine) , Grafts from AA-affected C3H/HeJ mice onto C3H/SmnC Prkdc(scid)/J mic e resulted in depigmented hair fiber regrowth and perifollicular neutr ophil and eosinophil infiltrates but no hair loss (15 of 15). Sham gra fting did not induce AA (none of 10), The finding that AA can be seria lly transferred from AA-affected C3H/HeJ mice to normal littermates an d C3H/OuJ mice, indicates that an immune response against hair follicl es can be induced with suitable stimuli. Conversely, skin grafts from normal C3H/HeJ, of C3H/SmnC Prkdc(scid)/J, mice rapidly lose hair due to lymphocyte, but not neutrophil and eosinophil, mediated inflammatio n. This AA induction method reproducibly provides large numbers of AA- affected mice to study the pathogenesis and treatment of human AA.