Lichen Planus: Pathogenesis, Subtypes, Comorbidities, and Emerging JAK Inhibitor Treatments

Conclusions

• Lichen planus is best understood as a lichenoid, T-cell–mediated inflammatory disease with shared pathogenic pathways across cutaneous, mucosal, nail, and follicular subtypes.
• Across studies, IFN-gamma–dominant type 1 immune signaling and STAT1 activation appear to be central drivers of lichen planus inflammation.
• A distinct CD8+CXCL13+ T-cell population likely plays a key pathogenic role in lichen planus by promoting cytotoxicity and sustaining keratinocyte injury.
• Lichen planus often behaves as a multisystem disease with important mucosal, ocular, esophageal, otic, and genital involvement that requires multidisciplinary evaluation.
• Patients with lichen planus have meaningful systemic comorbidity burden, including increased associations with cardiovascular and other autoimmune diseases.
• Conventional therapies such as potent topical steroids and various systemic agents are often insufficient, with a substantial fraction of patients remaining refractory to treatment.
• Apremilast, dupilumab, and secukinumab have not emerged as consistently effective broad treatments for lichen planus.
• JAK inhibition, especially JAK1-targeted therapy and related JAK/TYK2 inhibition, is the most promising emerging treatment strategy across multiple lichen planus subtypes.
• Early reports suggest topical ruxolitinib and oral baricitinib can produce marked clinical improvement and reduce pathogenic immune pathways.
• The overarching conclusion is that future lichen planus management should move from nonspecific immunosuppression toward pathway-directed therapy based on interferon-driven disease biology.