Defective expression of adhesion molecules on human bladder tumour and human tumour cell lines.

The pattern of expression of cell adhesion molecules, i.e., leucocyte function associated antigen 3 (LFA-3) and intercellular adhesion molecule 1 (ICAM-1) on human bladder tumour biopsy specimens was investigated. Attempts were also made to study the pattern of induction of these molecules by established human cell lines in response to cytokines. The results indicated that 15 of 25 tumour biopsy specimens were negative for ICAM-1, and amongst the remaining 10, only 1 showed strong positivity, whilst LFA-3 was expressed in 21 of 23 cases. Unlike LFA-3, the pattern of ICAM-1 expression on established tumour cell lines was different in that there were 7 of 21 cases showing positive staining. The parallel investigation of ICAM-1 and major histocompatibility complex class II antigen expression on bladder tumours showed that in 11 of 18 cases, there was a concomitant expression or complete absence of these molecules. In the remaining 7, there were 6 cases where only class II expression was observed. Exposure of cell lines to interferons alpha or gamma had no effects on LFA-3 expression. In contrast, interferon gamma induced ICAM-1 on all the eight lines with constitutive ICAM-1 expression, whereas interferon alpha upregulated only 2 of these 8 lines. The mean +/- SD values for ICAM-1 expression on the eight inducible lines were 617 +/- 406 cpm before and 943 +/- 471 cpm (p = 0.001) after interferon gamma stimulation. The pattern of ICAM-1 inducibility of a bladder cell line Fen to interferon remained unchanged following transfection of a beta2-microglobulin gene and correction of cell surface HLA class I antigens. These results indicate that there was a significant minority of bladder tumours and tumour cell lines with abnormal cell adhesion molecule expression. In some cases, the abnormality in cell lines could not be corrected by cytokine stimulation. It is possible that these abnormalities may play a critical role in the overall tumour strategy for escape from immunological detection.