Differential Effect of IL-4 and IL-13 on CD44 Expression in the Burkittʹs Lymphoma B Cell Line BL30/B95-8 and in Epstein–Barr Virus (EBV) Transformed Human B Cells: Loss of IL-13 Receptors on Burkittʹs Lymphoma B Cells

IL-4 and IL-13, cytokines with similar biological effects may influence growth and progression of B-cell tumors through regulation of key cell surface molecules important in intercellular communications. In this study, we demonstrate that IL-4 and IL-13 exhibited differential effects on CD23 and CD44 expression and binding to hyaluronan in BL30/B95-8, a Burkittʹs lymphoma (BL), and MK3.31, an Epstein–Barr virus transformed normal human B cell line (B-LCL). Studies conducted to understand the molecular mechanisms underlying this differential effect show that IL-4 induced phosphorylation of JAK1, JAK3, and STAT6 in BL30/B95-8 cells and of JAK3 and STAT6 in MK 3.31 cells. In contrast, IL-13 failed to induce the phosphorylation of JAK kinases or STAT6 proteins in these cell lines. The inability of BL30/B95-8 cells to respond to IL-13 was attributed to the loss of expression of IL-13R subunits α1 and α2, a finding confirmed for a number of other BL cell lines examined.