Expression of ICAM-1 on Short-Term Cultured Human Keratinocytes: Modulation by IFN-gamma, UVB and retinoic acid

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.