Lichen planopilaris (LPP) is one of scarring alopecias that presents chronic lymphocytic inflammation around the hair follicle and subsequent hair loss and scar formation. Langerhans cells (LCs) are absent in the epidermis of scar of LPP. However, the underlying mechanism of LC loss in LPP are still unknown. The purpose of this study is to investigate the alteration of expression of some proteins that are associated with LC development and maintenance such as TGF-β, IL-34, BMP-7, integrin (ITG) αvβ6 and ITG αvβ8 using skin samples from LPP patients by immunohistochemistry. LCs were diminished in LPP scar epidermis, but not LPP folliculitis epidermis. Although we expected that TGF-β was downregulated in LPP scar epidermis, TGF-β was not downregulated in LPP scar epidermis compared with normal epidermis and LPP folliculitis epidermis. Additionally, the expression of IL-34, Bone Morphogenetic Protein-7 (BMP7), and ITG αvβ8 was not also altered. Only ITG αvβ6 was apparently downregulated in LPP scar epidermis. ITG αvβ6 is crucial for the maintenance of epidermal LCs by facilitating the processing of inactive LAP TGF-β derived from LCs into active TGF-β. Next, we examined the specificity of loss of LCs and downregulation of ITG αvβ6 in LPP scar epidermis among other scar formation diseases. The number of LCs in the epidermis was comparable in DLE and was upregulated in hypertrophic scar and keloid compared with normal epidermis. Furthermore, the expression of ITG αvβ6 in the epidermis was comparable in these scar diseases compared with normal epidermis. These data suggested that loss of LCs is specific for LPP among scar formation diseases and the downregulation of ITG αvβ6 in scar epidermis may trigger LC loss. The expression of ITG αvβ6 in LPP folliculitis epidermis was not downregulated compared with normal hair follicles. Accordingly, some events occurring from folliculitis stage to scar formation seem to result in the downregulation of ITG αvβ6, followed by LC loss due to lack of active autocrine TGF-β derived from LCs.

Loss of Langerhans cells in scar lesion of lichen planopilaris is caused by downregulation of integrin αvβ6 in the epidermal keratinocytes