Irish journal of medical science · 2025
Immunohistochemical investigation of transferrin receptor 2 (TFR2) immunoreactivity in patients with cutaneous lichen planus.
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Celik Mehmet Semih, Asır Fırat, Aktas Hamza, Cetin Alpay, Celik Candan, Cepik Nagehan, Kaya Sibel, Akdeniz Ayşenur Sevinç, Yıldırım Esma
Аннотация
BACKROUND AND AIM: Lichen planus (LP) is a chronic inflammatory dermatosis with an unclear pathogenesis. Recent studies suggest that iron metabolism, oxidative stress, and ferroptosis mechanisms may play a role in the development of LP. Transferrin Receptor 2 (TFR2), an important receptor in iron homeostasis, may contribute to these processes.
METHODS: TFR2 immunoreactivity was evaluated using immunohistochemical methods on skin biopsies obtained from patients diagnosed with cutaneous LP (n = 45) and healthy controls (n = 30). Staining intensity was measured with QuPath image analysis software using 3,3'-diaminobenzidine (DAB). In addition, histopathological findings and staining localization were examined.
RESULTS: In healthy skin samples, TFR2 expression was limited, showing only weak staining in the basal epidermis and mild cytoplasmic positivity around the dermal vasculature (mean DAB intensity: 22.0% ± 5.5). In contrast, LP lesions exhibited pronounced epidermal irregularities, hyperkeratosis, inflammatory infiltration, and significantly increased TFR2 expression (mean DAB intensity: 57.0% ± 5.9; p < 0.05). Notably, strong cytoplasmic staining was observed in the epidermal basal layer and dermal inflammatory cells.
CONCLUSION: This study demonstrated a significantly increased expression of TFR2 in LP lesions compared to healthy skin. The findings suggest that TFR2 may contribute to the pathogenesis of LP through the ferroptosis mechanism mediated by oxidative stress. However, further advanced studies evaluating specific markers related to ferroptosis are needed to better clarify this relationship.
METHODS: TFR2 immunoreactivity was evaluated using immunohistochemical methods on skin biopsies obtained from patients diagnosed with cutaneous LP (n = 45) and healthy controls (n = 30). Staining intensity was measured with QuPath image analysis software using 3,3'-diaminobenzidine (DAB). In addition, histopathological findings and staining localization were examined.
RESULTS: In healthy skin samples, TFR2 expression was limited, showing only weak staining in the basal epidermis and mild cytoplasmic positivity around the dermal vasculature (mean DAB intensity: 22.0% ± 5.5). In contrast, LP lesions exhibited pronounced epidermal irregularities, hyperkeratosis, inflammatory infiltration, and significantly increased TFR2 expression (mean DAB intensity: 57.0% ± 5.9; p < 0.05). Notably, strong cytoplasmic staining was observed in the epidermal basal layer and dermal inflammatory cells.
CONCLUSION: This study demonstrated a significantly increased expression of TFR2 in LP lesions compared to healthy skin. The findings suggest that TFR2 may contribute to the pathogenesis of LP through the ferroptosis mechanism mediated by oxidative stress. However, further advanced studies evaluating specific markers related to ferroptosis are needed to better clarify this relationship.