Alopecia areata: an autoimmune disease?

A wide range of hypotheses such as focal infection, trophoneuroses, and end ocrine dysfunction, have been previously proposed to explain the pathogenes is of alopecia areata (AA). Currently, the most widely held belief is that AA is an autoimmune disease with cellular; and/or humoral immunity directed against anagen hair follicle antigen(s). However, until recently evidence in support of an autoimmune mechanism of AA has been largely circumstantial . More fundamental evidence has recently been amassed in support of AA as a n autoimmune disease by using animal models. These data include: 1) identif ication of cross-species hair follicle specific IgG autoantibodies, 2) The ability to induce AA in an animal model with transfer of skin from affected to naive individuals, and 3) the induction of disease by transfer of lymph ocytes to human skin grafted to severe combined immunodeficiency mutant mic e. A review of the previous and current data related to the autoimmune basi s of AA is provided to put into perspective the future studies needed to de finitively determine whether AA is an autoimmune disease.