Abstract

Alopecia areata (AA) is an autoimmune disease characterized by T cell infiltration of the hair follicle. The breakdown of tolerance to the hair follicle is thought to be the driving force in the nonscarring hair loss seen in patients. There are currently no FDA approved treatments for AA. IL-27 plays a pleotropic role across many other autoimmune diseases; however, whether its immunoregulatory effects can be leveraged for therapeutic applications in AA is unknown. To address this, we used an adeno-associated virus (AAV) that drives overexpression of IL-27 in our C3H/HeJ skin graft-induction model of AA.

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