Rebound effect associated with JAK inhibitor use in the treatment of alopecia areata

Abstract

Alopecia areata (AA) is a common autoimmune disease driven by Th1 cytokines characterized by non‐scarring hair loss.^1,2 Mouse models have demonstrated that IFN‐γ‐producing NKG2D+ CD8+ cytotoxic T lymphocytes (CTLs) are essential for disease pathogenesis, along with JAK‐STAT dependent cytokines IFN‐γ and IL‐15, which induce autoreactive T cell activation.^1,3

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