Knowledge of the disease mechanisms in alopecia areata is discussed in
the Light of progress in hair biology, immunology, and genetics. A di
sease model is presented incorporating polygenic determination of dise
ase severity and susceptibility with largely unknown trigger factors r
esponsible for initiating clinical disease expression. Experimental sy
stems including animal models for alopecia areata offer new opportunit
ies for investigation of alopecia areata and developing novel therapie
s.