Lichen planus (LP) is an auto-inflammatory skin disorder identified by a presence of T-cell lymphocytes at the dermal-epidermal junction. It is hypothesized that the INF-γ/CXCL10 axis fulfills a major role in the onset and persistence of chronic inflammation in LP. Since Janus kinases (JAKs) are involved in the transduction of INF-γ signals, they may be good targets for LP treatment. Several case reports and case series described the safety and efficacy of upadacitinib (2 articles), tofacitinib (6 articles), baricitinib (4 articles), and Ruxolitinib (1 Article) in the treatment of LP variants. The predominant variants that JAK inhibitors improved were lichen planopilaris, nail LP, and erosive LP. Considering the role of the JAK pathway in LP pathogenesis and the evidence provided by these reports, it seems JAK inhibitors would be effective therapeutic agents for LP treatment. Hence, these agents should be trialed and evaluated further.
Keywords: JAK inhibitors; JAK pathway; Lichen planus; barcitinib; ruxolitinib; tofacitinib; upadacitinib.