Expression of interferon‐gamma receptors and interferon‐gamma‐induced up‐regulation of intercellular adhesion molecule‐1 in basal cell carcinoma; decreased expression of IFN‐γR and shedding of ICAM‐1 as a means to escape immune surveillance

Abstract

The peritumoural inflammatory infiltrate in basal cell carcinoma (BCC) of the skin consists mainly of T lymphocytes which hardly invade the tumour nests. The absence of intercellular adhesion molecule-1 (ICAM-1) on BCC cells may explain the lack of tumour-infiltrating cells and the lack of an active cell-mediated immune response in this tumour. In this study, the induction of ICAM-1 was investigated in BCC biopsies using recombinant human interferon-gamma (rHuIFN-γ). The expression of interferon-gamma receptors (IFN-γR) in the biopsies was also investigated. The results showed that BCC cells expressed ICAM-1 after incubation with rHuIFN-γ, but to a lesser degree than normal epidermal cells. The levels of shed ICAM-1 were significantly increased in the culture supernatants of tumour biopsies compared with those from normal skin biopsies, after culturing in the presence of rHuIFN-γ. The expression of IFN-γR was significantly decreased on the tumour cells compared with the overlying epidermis. The decreased expression of IFN-γR on the tumour cells and the shedding of ICAM-1 into the peritumoural stroma may be a plausible mechanism by which the tumour cells are protected against an active cell-mediated immune response. © 1998 John Wiley & Sons, Ltd.