Pathophysiology of Alopecia Areata in the Pediatric Patient

Alopecia areata (AA) is an autoimmune non-scarring hair loss that arises in genetically susceptible individuals, potentially in combination with environmental triggers or inciting events, of which the exact mechanism is not yet fully understood. Genome wide association studies have demonstrated an association between AA and variants in HLA haplotypes on chromosome 6 which correlate with other autoimmune conditions as well as other gene variants. Familial and twin studies also confer additional evidence to a genetic component. AA pathogenesis relies on immune privilege collapse at the hair follicle (HF) bulb in the anagen hair cycle phase. Immune privilege collapse is associated with upregulation of IFN-γ, ultimately activating JAK-STAT pathway resulting in upregulation of MHC class I and II in the HF and subjecting it to attack by NKG2D⁺ CD8 T cells. The complex interplay between pro-inflammatory cytokines such as IFN-γ, IL-2, IL-15 and their use of JAK-STAT signaling are important in perpetuation of AA.