Alopecia Areata: A Review of Disease Pathogenesis

F. Rajabi; L.A. Drake; M.M. Senna; N. Rezaei

Disclosures

The British Journal of Dermatology. 2018;179(5):1033-1048. 

In This Article

Pathogenesis Overview

Many theories have been developed regarding the aetiology of AA since its description by Sauvages in 1760. Initially, the involvement of an infectious or toxic agent was considered causative, then neuropathic and endocrine disturbance theories were presented.[11] Finally, in the 1960s, the autoimmunity hypothesis gained popularity.[12,13] The concept of autoimmunity in AA is supported by the high rate of association with other immune-mediated diseases like vitiligo and thyroiditis, and the response seen to immune-modifying treatments.[14–16] Nonetheless, the common autoimmune pathways like cross-reactive antigens, haptenization and genetic mutations are not considered influential.[17] The pathophysiological hypothesis for AA mainly emphasizes the loss of the HF immune privilege (IP).

Like other autoimmune diseases, a genetic predisposition for AA has also been suggested by observational studies reporting familial clustering, twin studies and genome-wide association studies.[18–20] The genes implicated in AA development are listed in Table 1.

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