Objectives: To investigate lesions from patients with LPP with regard to differences in the pattern of expression of some immuno-histochemical markers which may explain the pathogenesis of scarring process, which characterize this disease.
Methodology: Skin biopsies from twelve LPP patients were studied for cells expressing CD3, CD4, CD8, CD20, and CD68. They were stanied by double immunohistochemeistry means for the expression of cutaneous lymphocyte antigen (CLA) and the cytotoxic molecule, granzyme B.
Results: Double staining lesions revealed that the granzyme B-expressing lymphocytes were mostly of the CLA+ skin-homing phenotype, and the increased expression of granzyme B in LPP was associated histologically with the inflammatory infiltrate that involved the epidermis and the adnexal structures. The cellular infiltrate was demonstrated at the vicinity of the dermoepidermal junction and may be involved in the destruction of the overlying epidermis with secondary abnormal healing of the epidermis, secondary scarring and fibrosis.
Conclusions: This study provides an evidence of potentially autoreactive cytotoxic T-lymphocytes targeting adnexal structures in association with scarring LPP. It is, therefore, possible that these cells are responsible for scar formation. (Rawal Med J 2014;39: ).
Key words: Lichen Planopilaris, Inflammatory cell infiltrate, immunohistochemistry.
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