# Notable Differences in Clinical Features and Inflammatory Gene Expression Between Genital Lichen Sclerosus and Lichen Planus

**Authors:** Patrick Poffet, Veronika Baghin, Fabienne Fröhlich, Irina Banzola, Julia Laube, Mark Mellett, Lucie Heinzerling, Barbara Meier-Schiesser

PMC · DOI: 10.3390/biomedicines13112817 · 2025-11-19

## TL;DR

This study compares genital lichen sclerosus and lichen planus, finding differences in age, gender, comorbidities, and inflammatory gene expression patterns.

## Contribution

The study identifies distinct inflammatory gene profiles and clinical features between genital lichen sclerosus and lichen planus.

## Key findings

- LS patients were older, predominantly female, and more likely to have metabolic syndrome compared to Lpg patients.
- LS showed upregulated CCL27 and MARCO, while Lpg exhibited IL-1 pathway activation and B-cell markers.
- The findings reveal distinct immunological profiles that could guide targeted therapies for each condition.

## Abstract

Background/Objectives: Genital lichen sclerosus (LS) and lichen planus genitalis (Lpg) are chronic inflammatory dermatoses with overlapping clinical features but incompletely understood pathogenesis. Current therapies are largely symptomatic. Methods: To clarify underlying mechanisms and identify therapeutic targets, we retrospectively analyzed 174 patients (142 LS and 32 Lpg). Clinical features and comorbidities were compared, and gene expression profiling of 730 inflammation-related genes was performed on lesional tissue from LS and Lpg patients and healthy controls using NanoString technology. Selected findings were validated by immunohistochemistry. Results: LS patients were older and predominantly female and more frequently had metabolic syndrome. On the molecular level, LS showed a generally lower inflammatory gene expression profile than Lpg. Nevertheless, LS was characterized by strong upregulation of CCL27 and MARCO, whereas Lpg displayed enhanced IL-1 pathway activation and increased expression of B-cell–associated markers. Conclusions: These results demonstrate distinct immunological differences between the two conditions and provide further insight into disease-specific pathways.

## Linked entities

- **Genes:** CCL27 (C-C motif chemokine ligand 27) [NCBI Gene 10850], MARCO (macrophage receptor with collagenous structure) [NCBI Gene 8685]
- **Diseases:** metabolic syndrome (MONDO:0000816)

## Full-text entities

- **Genes:** IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, CCL27 (C-C motif chemokine ligand 27) [NCBI Gene 10850] {aka ALP, CTACK, CTAK, ESKINE, ILC, PESKY}, MARCO (macrophage receptor with collagenous structure) [NCBI Gene 8685] {aka SCARA2, SR-A6}
- **Diseases:** metabolic syndrome (MESH:D024821), Inflammatory (MESH:D007249), Genital Lichen Sclerosus (MESH:D018459), inflammatory dermatoses (MESH:D012871), Lichen Planus (MESH:D008010)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12650408/full.md

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Source: https://tomesphere.com/paper/PMC12650408