Oral Baricitinib in the Treatment of Cutaneous Lichen Planus
Hwang, A. S.; Kechter, J. A.; Do, T.; Hughes, A.; Zhang, N.; Li, X.; Wasikowski, R.; Brumfiel, C.; Patel, M. H.; Boudreaux, B.; Bhullar, P.; Nassir, S.; Yousif, M.; DiCaudo, D. J.; Fox, J.; Gharaee-Kermani, M.; Xing, X.; Zunich, S.; Branch, E.; Kahlenberg, J. M.; Billi, A.; Plazyo, O.; Tsoi, L. C.; Pittelkow, M. R.; Gudjonsson, J. E.; Mangold, A. R.
Show abstract
BackgroundCutaneous lichen planus (LP) is a recalcitrant, difficult-to-treat, inflammatory skin disease characterized by pruritic, flat-topped, violaceous papules on the skin. Baricitinib is an oral Janus kinase (JAK) 1/2 inhibitor that interrupts the signaling pathway of interferon (IFN)-{gamma}, a cytokine implicated in the pathogenesis of LP. MethodsIn this phase II trial, twelve patients with cutaneous LP received baricitinib 2 mg daily for 16 weeks, accompanied by in-depth spatial, single-cell, and bulk transcriptomic profiling of pre-and post-treatment samples. ResultsAn early and sustained clinical response was seen with 83.3% of patients responsive at week 16. Our molecular data identified a unique, oligoclonal IFN-{gamma}, CD8+, CXCL13+ cytotoxic T-cell population in LP skin and demonstrate a rapid decrease in interferon signature within 2 weeks of treatment, most prominent in the basal layer of the epidermis. ConclusionThis study demonstrates the efficacy and molecular mechanisms of JAK inhibition in LP. Trial Registration Number: NCT05188521
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