Abstract

Intercellular adhesion molecule I(ICAM-1; CD 54), a 90 kD glycoprotein, counter-receptor for lymphocyte function-associated antigen-I(LFA-1) on T-cells, is critically important to a wide variety of adhesion-dependent leukocyte functions, including antigen presentation and target cell lysis. Induction of ICAM-1 on the keratinocytes(KCs) is an important regulator in initiation, maintenance, and resolution of cutaneous inflammation, which is modulated with cytokines produced by activated T-lymphocytes. This study was designed to further our understanding on modulation effects of ultraviolet B(UVB), gamma interferon(IFN-;v), and retinoic acid(all trans) upon expression of ICAM-1 on cultured human KCs, with emphasis on their correlation. Cell surface expression of ICAM-1 in cultured human KCs was analyzed with the use of indirect immunofluorescence and fluorescence activating cell sorting(FACS) by flow cytometry. The results of this study were as follows: 1) Expression of ICAM-1 was significantly induced with IFN-,-(20 U/ml)(p<0.005). 2) UVB irradiation of 30mJ/cm2 significantly suppressed ICAM-1 expression of KCs 24 hours after irradiation(p<0.05). However, at 72 hours after irradiation, ICAM-1 expression of KCs was considerably increased in comparison to that of initial phase (24 hours after irradiation). 3) High concentrations(10(-5)M) of retinoic acid reduced UVB-induced expression of ICAM-1 in late phase(72 hours after irradiation), although retinoic acid showed induction effect of ICAM- I expression of KCs. In summary, these results indicate that ICAM- I may contribute to the biphasic effect of UVB on delayed hypersensitivity in vivo. Also, retinoic acid, a vitamin A derivative, may have a cutaneous photoprotective effect through a regulation of UVB-induced ICAM-1 expression on the KCs.

• Keywords: intercellular adhesion molecule-1;Keratinocytes;Ultraviolet B;Gamma interferoii;Retinoic acid