their coexistence.2,11 Increased ROS is an anticipated trigger of the innate immune system in both diagnoses. Genome-wide association studies have demonstrated both innate and adaptive immunity, and mechanistic studies in mouse models have
implicated an IFN-γ driven immune response and cytotoxic CD8+ T cells as chief pathogenic factors.9
Furthermore, statistics show IFN-γ, IL-1B, and IL-6 serum levels are significantly elevated in AA and NSV patients when compared
to healthy controls.10 Upregulation of several JAK-STAT pathway components downstream of gamma chain containing cytokines
in the shared etiopathogenetic pathways. IFN-γ and γc cytokines, including IL-2, IL-7, and IL-15 are notorious for augmenting AA
disease with studies highlighting that IFN-γ signals primary through JAK1/2 and IL-15 mostly via JAK1/3.22,23
