Pathophysiology of Alopecia Areata in the Pediatric Patient

Alopecia areata (AA) is an autoimmune condition causing non-scarring hair loss, influenced by genetic susceptibility and possibly environmental factors. Genome-wide association studies link AA to HLA haplotypes on chromosome 6 and other gene variants, suggesting a genetic component supported by familial and twin studies. The pathogenesis involves the collapse of immune privilege at the hair follicle bulb during the anagen phase, with upregulation of IFN-γ activating the JAK-STAT pathway. This leads to increased MHC class I and II expression, making the hair follicle vulnerable to attack by NKG2D⁺ CD8 T cells. The interaction of pro-inflammatory cytokines like IFN-γ, IL-2, and IL-15, and their JAK-STAT signaling, plays a crucial role in the persistence of AA.