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

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.