RESUMO
The Burkitt lymphoma-derived Daudi cell line is often used as an in vitro model for germinal center B-cell function. Globotriaosyl ceramide (CD77), a marker for germinal center B-cells, is present on Daudi cells but is deficient in the Daudi-derived mutant VT500 cell line. Previous results showed a correlation in these cells between CD77 expression and expression of the B-cell protein CD19 and indicated that CD19/CD77 interaction is a mechanism for B-cell adhesion. Roles for CD77 in IFN-alpha-induced growth inhibition and anti-viral activity also have been described previously. Through flow cytometric analysis and adhesion assays, we investigated whether expression of CD77 was required for cell adhesion pathways induced by IFN or antibodies against additional B-cell surface molecules: CD20, CD22, CD38, CD40, CD81 and HLA-D proteins. In contrast to the pronounced homotypic adhesion induced by treatment with interferon-alpha in Daudi cells, no increase in adhesion was observed in IFN-treated VT500 cells. Of the B-cell proteins tested, only CD22-mediated adhesion and surface expression was stronger in Daudi than in VT500 cells. These results indicate that CD77 may be required for IFN and CD22-associated adhesion pathways, but CD77 is not a universal component of adhesion pathways in these cells.
