The distribution and intracellular location of Fas and Fas Ligand following gastric carcinogenesis: Fas Ligand expressing gastric carcinoma cells can inhibit local immune response.

Previous reports indicated that Fas Ligand (FasL) in gastric carcinoma might support tumour cells to evade host immune attack. However, the mechanism induced by the Fas/FasL system has not yet been described on the basis of comparison of normal and malignant tissues in terms of the features of regional location of Fas and FasL. By using immunostaining methods, we studied the distribution and regional location of Fas and FasL in gastric epithelial cells (GECs), gastric carcinoma cells (GCCs), normal gastric stroma-infiltrating lymphoid cells (NGILs) and tumour-infiltrating lymphoid cells (TILs) in 59 tissue specimens of human gastric carcinoma. The expression of Fas within the entire GECs was higher than that in all GCCs (P < 0.0001); however, the expression of Fas in NGILs was lower than that in TILs (P < 0.0001). The expression of FasL showed no significant difference between GECs and GCCs, or between NGILs and TILs. When we analyzed the Fas/FasL expression on cytomembrane (CM) in GECs and GCCs, Fas-in-CM was detected in 79.4% and 33.33% (P < 0.05), compared with 3.03% and 56.67%, respectively, for FasL-in-CM (P < 0.001). Our results suggest that there is indeed a possible mechanism to assist cancer cells to evade host immune attack, and this mechanism depends on the dynamic state of Fas/FasL expression, that is, Fas showed a tendency to be expressed within the cells, whereas FasL showed a tendency to be expressed on the cell membrane following carcinogenesis.