Fig. 6

The potential of C26 cells to activate LSECs is mediated by tumor LFA-1 expression. Uptake of TRITC-labeled mannan (a) after stimulation with either C26 cells (grey bar) or β₂-C26 cells (white bar) was quantified. Data are presented as % of internalized uptake by LSECs activated by either C26 or β₂-C26 cells compared to that of LSECs cultured alone. b The expression of genes involved in the ability of C26 to altered Mannose receptor upregulation after ligation of LFA-1 with endothelial ICAM-1 was analyzed by quantitative PCR in tumor cell lysates after sICAM-1 (200 ng/m) stimulation. Data of RNA expression are presented as C26 cells gene expression relative to sICAM-1 activated C26 cells gene expression (dark bars) and β₂-C26 cells gene expression relative to sICAM-1 activated β₂₋C26 cells gene expression (white bars). c DQ-ovalbumin processing by LSECs (short dash line) was quantified after stimulation with either C26 cells (continuous line) or β₂-C26 cells (long dash line). Data are presented as AFU -arbitrary fluorescence units. Data are mean values ± SD from three different experiments. Changes were considered statistically significant at *p < 0.05. d Activation of LSECs by C26 cells with partial expression of β₂integrin does not affect lymphocyte cytotoxic activity towards C26. Liver sinusoidal lymphocytes (LSLs) were incubated for 24 h with either untreated LSECs, or LSECs activated with C26 or β₂-C26 cells. Then, LSLs were transferred to C26 cultures and co-incubated for another 24 h. Subsequently, their cytotoxic activity towards C26 cells was measured by the Presto Blue assay. Basal untreated LSLs (left bar) were used to quantify basal cytotoxic activity of LSLs towards C26 cells. Data are mean values ± SD from three different experiments. Changes were considered statistically significant at *p < 0.05