Samantha Shao, BA: No financial relationships to disclose
Introduction/Rationale: Cutaneous lichen planus (cLP) is a T cell–mediated skin disease in which cytotoxic CD8⁺ T cells attack basal keratinocytes at the dermo-epidermal junction. While studies have characterized T cell subsets in lesional tissue, circulating immune signatures in cLP are incompletely defined. We performed deep immunophenotyping of circulating T-cell subsets to map systemic alterations in cLP patients vs healthy controls.
Methods: We included 12 treatment-refractory cLP patients (mean age 63.6 ± 13.6 years) and 2 healthy controls (37.5 ± 10.6 years). Whole blood was profiled for 27 markers by flow cytometry. Sequential gating: singlets → live → CD3⁺ T cells → CD4⁺/CD8⁺/γδ; FOXP3⁺ Tregs were defined within CD4⁺. Frequencies were expressed as % of the immediate parent population. Group comparisons used two-tailed exact Mann–Whitney tests with Hodges–Lehmann median differences.
Results: Across frozen specimens, cLP patients exhibited broad T-cell activation. Proliferation increased in CD4 (Ki67⁺, p< 0.05), CD8 (6.785% vs 0.885%; Δ=5.90; p< 0.05), and Tregs (83.0% vs 46.8%; Δ=34.1; p< 0.05). Intracellular CTLA-4 was higher on CD4 (11.07% vs 2.615%; Δ=8.45; p< 0.05), CD8 (21.05% vs 9.30%; Δ=11.6; p< 0.05), and γδ T cells (47.20% vs 24.45%; Δ=22.75; p< 0.05). CXCL13⁺ cells expanded in CD4 (28.20% vs 12.45%; Δ=15.5; p< 0.05), CD8 (18.05% vs 3.595%; Δ=14.46; p< 0.05), γδ (2.805% vs 0.465%; Δ=2.285; p< 0.05), and Tregs (7.56% vs 1.17%; Δ=6.39; p< 0.05). Tregs were TBET-high (78.75% vs 61.55%; Δ=17.3; p< 0.05); GITR⁺ Tregs trended up (p=0.1978).
Conclusion: cLP blood displays a CXCL13⁺, proliferative T-cell signature with increased intracellular CTLA-4 across CD4, CD8, γδ, and Treg compartments. CXCL13 elevation aligns with lesion-level literature implicating CXCL13⁺ CD8+ T cells that are suppressed in JAK-STAT therapy responders. Tregs exhibit a GITR upregulated, Th1-like phenotype that suggests loss of suppressive capacity, warranting further investigation on whether Treg dysfunction plays a causative role in cLP.
