TYK2 Inhibition with Deucravacitinib Improves Clinical Outcomes and Resolves Interferon-Driven Inflammation in Lichen Planopilaris
Stockard, A.; Leibovit-Reiben, Z.; Hu, B.; Jiang, R.; Roberts, B. T.; Penner, S.; Li, X.; Ramirez, Z.; Stewart, K.; Fox, J.; Bogle, R.; Zhang, N.; Shao, S.; Borges Da Silva, H.; DiCaudo, D. J.; Zunich, S.; Pincelli, T. P.; Tsoi, L. C.; Pittelkow, M. R.; Sluzevich, J.; Gudjonsson, J. E.; Mangold, A. R.
Show abstract
Lichen Planopilaris (LPP) is a lymphocyte-mediated scarring alopecia characterized by progressive follicular destruction and fibrosis. In this clinical trial, patients with biopsy proven LPP were treated with deucravacitinib (an oral inhibitor of tyrosine kinase 2 (TYK2)) 6 mg BID for 24 weeks (NCT-06091956). Bulk and single-cell RNA sequencing was performed on paired pre- and post-treatment scalp biopsies from baseline and week 4. Patients (N=10) demonstrated improvements in PGA (88.9%, p=0.008), LPPAI (-2.3 points, SD 1.1, p=0.002) and Skindex-16 (-21.0 points, SD 22.1, p=0.014) scores at week 24. Bulk transcriptomic analysis of untreated LPP revealed upregulation of type I Interferon (IFN)-stimulated genes and pathways related to inflammation, immune activation, keratinization, and extracellular matrix remodelling, with downregulation of immune and inflammatory pathways following treatment. Single-cell RNA-seq of LPP was characterized by enrichment of CD8+GZMK+ T cells which showed downregulation of T-cell receptor signaling as well as antiviral pathways with treatment. Basal keratinocytes exhibited reduced cytokine and interferon signaling and decreased communication with NK cells following treatment. CCL19+ fibroblasts were prominent in untreated disease was attenuated after treatment, with downregulation of type I IFN signaling. Selective TYK2 inhibition with deucravacitinib effectively suppresses these inflammatory circuits in LPP and represents a promising therapeutic strategy.
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