Reduced expression of programmed cell death 1 and programmed cell death ligand 1 in infiltrating inflammatory cells of lichen planus without administration of immune checkpoint inhibitors.

Keratinocytes are the main targets of infiltrating T cells in the pathogenesis of lichen planus. However, the mechanisms of dense inflammatory infiltrates beneath the epidermis remain unknown. The aim of the present study was to clarify the roles of programmed cell death 1 (PD-1) and its ligand (PD-L1) in the pathogenesis of lichen planus. Immunohistochemistry of PD-1 and PD-L1 in 12 cases each of lichen planus and dermal-type erythema multiforme was performed. The expression of PD-1 and PD-L1 on infiltrating inflammatory cells, predominantly lymphocytes in lichen planus, was significantly less compared to that in dermal-type erythema multiforme. By dual immunofluorescence, the overlap between PD-1 and leukocyte common antigen, CD4, CD8, CD68, and factor XIIIa was limited and found in only a very small portion of lichen planus cells. Our data suggest that decreased expression of PD-1 and PD-L1 could play a role in accelerating inflammatory cell infiltration targeting the epidermis in the pathogenesis of lichen planus.