Abstract:
Alopecia areata is the most prevalent autoimmune disorder which causes non-scarring hair loss. It may increase the anxiety of patients and increase their chances of developing psychological and psychiatric disorders. There are two proposed theories for the pathogenesis of alopecia areata.
The most evidence-based hypothesis is an autoimmune reaction caused by collapse of hair follicle immune privilege, Immune privilege collapse is assumed to be either a primary event that triggers antigen presentation in a disturbed hair follicle environment, or an event that occurs as a result of dysregulation of central immune system that involves the follicles.
Several gene loci have been identified with alopecia areata. The key immune effectors in the pathogenesis include autoreactive effector T cells, natural-killer group 2, member (NKG2D) + CD8+cytotoxic T cells, natural killer (NK) cells, Janus kinase, signal transducers and activators of transcription (JAK/STAT) pathway, MHC-I chain-related gene A (MICA), interferon‐γ (IFN‐γ) and interleukin-15 (IL-15).
Alopecia areata has no accepted cure and has an unpredictable response to treatment. The recognition of the exact pathogenic mechanisms of alopecia areata is necessary to identify the potential therapeutic targets.
Key words: alopecia areata, pathogenesis, immune privilege.