The autoimmune basis of alopecia areata: a comprehensive review

Alopecia areata (AA) is a common, non-scarring dermatologic condition regularly distinguished by patches of hair loss on the scalp also manifesting in other, severe forms, including alopecia totalis (total loss of hair on the scalp) and alopecia universalis (complete loss of hair on the scalp and body). AA is a clinically heterogeneous disease with greatly varying yet typical symptoms, but the etiology for AA remains an enigma. However, clinical and experimental studies have pointed to autoimmune involvement, specifically regarding immune privilege sites of the hair follicles and the infiltration of CD4+ and CD8+ T cells and a predominant Th1 cytokine profile. Environmental insults, such as viral infections, trauma and genetic predisposition are also believed to contribute to the disease process. Multiple treatment options including the use of broad acting corticosteroids appear to be relatively effective in mild cases, however the clinical management of more severe forms of AA is much more difficult. Recent studies suggest that intervention of the JAK pathway may have a potential therapeutic efficacy for AA.