Alopecia Areata (AA) is a CD8+ T cell-mediated autoimmune disease that is directed against anagen-associated autoantigens which become exposed to the immune system following the collapse of the hair follicle’s physiological immune privilege, and presumably only when hair follicles undergo active growth, produce a hair shaft, and are engaged in pigment synthesis (anagen).

The mechanisms that contribute to the development of AA are currently under investigation. A major genome wide association study (GWAS) strongly supported the importance of NKG2D in AA, which had previously been suggested by immunohistological analyses. In a large cohort of AA patients, expression of the genes encoding the NKG2D agonists, MICA, and even more prominently so, the MICA family member ULBP3, was found to be strongly associated with AA. Members of the γc cytokine-receptor pathway have also been implicated in AA, suggesting a role for downstream signaling via JAK molecules, with increased JAK1 and JAK3 expression detected in lesional human and mouse skin. In fact, even though properly controlled, randomized, double-blind, and prospective clinical trials on these findings remain to be published, an impressive preventive and therapeutic effect of JAK inhibitors (e.g. Ruxolitinib or Tofacitinib) has been observed in AA patients. Most studies have demonstrated a key role of IFN-γ, which signals via the JAK pathway, as a major pathogenic cytokine in AA. However, other studies and preliminary clinical case reports have pointed to additional therapeutically targetable components of other pathways and cytokines including IL-15, IL-13 and IL-23.

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Sandra Jones

Journal Manager

Hair Therapy and Transplantation

Email: hairtherapy@emedscholar.com