IN 3 TYPES OF INTERFACE DERMATITIS, DIFFERENT PATTERNS OF EXPRESSION OF INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) INDICATE DIFFERENT TRIGGERS OF DISEASE

We found distinct patterns of intercellular adhesion molecule-1 (ICAM- 1) expression in three diseases characterized by interface dermatitis with mononuclear infiltrates and keratinocyte cytotoxicity: lichen pla nus (LP), subacute cutaneous lupus erythematosus (SCLE), and erythema multiforme (EM). In LP, basal keratinocytes show strong ICAM-1 express ion associated with a dermal infiltrate, but ICAM-1. expression in the rest of the epidermis is minimal, In SCLE, there is diffuse epidermal ICAM-1 expression, sometimes with accentuation on the cell surface of basal cells, In EM, there is strong basal cell expression of ICAM-1 w ith evident cell surface accentuation, and also pockets of suprabasal expression with cell surface accentuation. These patterns are associat ed with different factors that trigger cytokine release in different l ocations. Both tumor necrosis factor-alpha (TNF-alpha) and interferon- gamma (IFN-gamma) produce greater relative ICAM-1 expression in basal keratinocytes than in more differentiated keratinocytes, In LP, the pu re basal keratinocyte expression of ICAM-1 appears to be caused by cyt okines, predominantly IFN-gamma, released by dermal lymphocytes, The p attern of ICAM-1 in SCLE corresponds to the pattern induced by ultravi olet radiation (UVR): diffuse epidermal ICAM-1 expression, sometimes w ith basal accentuation. Some individuals are ''responders'' to TNF-alp ha or UVR, showing high levels of ICAM-1 expression following UVR or T NF-alpha stimulation in vitro or UVR stimulation in vivo. We propose t hat the pattern of ICAM-1 induction in SCLE is dependent on UVR-induce d TNF-alpha release.EM is associated with apparent latent Herpes simpl ex virus, and Herpes simplex virus (HSV)-infected keratinocytes show e nhanced ICAM-1 expression, We propose that in EM suprabasal ICAM-1 exp ression may be induced directly by HSV infection or indirectly through TNF-alpha release induced by HSV reactivation. Induction of ICAM-1 wi thin the epidermis is stratified and individually variable. Basal kera tinocytes show maximal induction of ICAM-1 expression due to innate se nsitivity to TNF and IFN-gamma stimulation, and to location adjacent t o dermal sources of cytokines, Suprabasal ICAM-1 can be induced by UVR and epidermal TNF-alpha release, and by factors such as viral infecti on. Different triggers of cytokine release and adhesion molecule induc tion may influence the different patterns of inflammation seen in dive rse inflammatory skin diseases.