engleski

Expression of the herpes virus entry mediator (HVEM), a member of the tumor necrosis factor receptor superfamily, in psoriasis and lichen planus

Background and Objective: The tumor necrosis factor receptor superfamily (TNFRSF) plays a major role in the development of immune responses. One of its members is the herpes virus entry mediator (HVEM), also known as TNFRSF14 or CD270. Initially identified as a cellular mediator of herpes simplex virus entry into cells, this membrane-bound receptor has been shown to bind several ligands that are capable of mediating T helper type 1 (Th1) responses. Its roles have been recognized in various inflammatory settings such as intestinal inflammation, experimental autoimmune encephalomyelitis and bacterial infections. Moreover, as a result of recent genome wide association studies, HVEM has been reported as a risk gene in inflammatory bowel disease. Objective of our study was to investigate the expression of HVEM in two prototype inflammatory diseases of the skin characterized by Th1 response, psoriasis and lichen planus. Methods: Immunohistochemistry for HVEM was performed on biopsies of lesional skin of patients with plaque psoriasis and lichen planus (n=10 per group). Double immunofluorescence was employed to examine the expression of HVEM among the populations of cells comprising the inflammatory infiltrate. The study was approved by the institutional ethics committee. Results: Immunohistochemical staining for HVEM was detected both in the epidermis and dermis. In lichen planus, staining was significantly stronger in lesional than in the corresponding non- lesional epidermis, and it was stronger in lower two thirds of the lesional epidermis. In psoriasis, an opposite pattern was observed, with less pronounced staining in lower, proliferating layers of epidermis. Moreover, mostly membranous staining was detected in lichen planus whereas in psoriasis cytoplasmic staining prevailed. HVEM+ cells were identified in a varying number within the psoriatic and lichenoid infiltrate. HVEM was expressed by a wide range of cell populations, but mostly by CD8+ lymphocytes and macrophages. Conclusions: The observed differences in the pattern of epidermal expression of HVEM between psoriasis and lichen planus as well as its presence on various cells of the inflammatory infiltrate in both skin pathologies indicate a possible role of HVEM-mediated signaling in the pathogenesis of inflammatory skin diseases and open a new area for future research. Limitations: Given the complexity of HVEM-induced signals mediated by its numerous ligands, these results are only a preliminary indication of the possible pathogenic role of HVEM- mediated responses in psoriasis and lichen planus.

Psoriasis; Lichen planus; HVEM; TNFRSF14

nije evidentirano