Abstract
Alopecia areata is a condition that affects hair follicles and leads to hair loss ranging from small well-defined patches to complete loss of all body hair. Despite its high incidence, the pathobiology is not fully understood, and no single concept could be universally accepted. Alopecia areata is mostly considered to be an autoimmune disease, in which the collapse of hair follicle immune privilege plays a key role. Higher incidence rate in the female population and increased overall risk of other autoimmune disorders militate in favor of autoimmune hypothesis. Antibodies against multiple components of hair follicles almost exclusively attack in anagen phase, where melanogenesis takes place. It suggests involvement of melanogenesis-associated autoantigens as a target epitope. Some investigators believed that alopecia areata is not a truly autoimmune disease but is only 'consistent with' autoimmune mechanisms. High frequency of a positive family history up to 42% may reflects the contribution of heredity factors. In addition, no specific target autoantigen has been identified so far, and autoantibodies to hair follicle-associated antigens are detectable in normal individuals.