IL-13 has only a subset of IL-4-like activities on B chronic lymphocytic leukaemia cells.

The recently described interleukin-13 (IL-13) has been shown to share many of the effects of IL4 on normal B cells, including growth-promoting activity and induction of CD23. In this study, we compared the effects of IL-13 and IL4 on B chronic lymphocytic leukaemias (B-CLL) cells. After anti-CD40 activation, both IL-13 and IL4 promoted the DNA synthesis of B-CLL cells and increased the recovery of viable cells. The time kinetics of the proliferative response of B-CLL cells to IL-13 or IL4 were superimposable and showed the long-lasting effect of both cytokines. As on normal B cells, both IL4 and IL-13 synergized with IL-10 to enhance B-CLL DNA synthesis. Moreover, IL-13, like IL-4, was able to increase CD23 expression on anti-CD40-activated leukemic B cells. The CD23 up-regulation and the DNA synthesis induced by IL-13 on anti CD40-activated B-CLL cells, were significantly reduced when B-CLL cells were cultured with anti-I L-4 receptor monoclonal antibody, suggesting a common pathway for IL-13 and IL-4 signalling. However, after cross-linking of surface IgM, IL-4 strongly inhibited the IL-2-induced DNA synthesis of B-CLL cells, whereas IL-13 did not inhibit IL-2-driven proliferation of anti-IgM-activated B-CLL cells. Furthermore, while IL-4 strongly up-regulated the expression of CD23 on anti-IgM-activated leukemic B cells, IL-13 only marginally increased it. Finally, IL-13, in contrast to IL-4, did not prevent the entry of B-CLL cells into apoptosis. Thus IL-13 and IL-4 display comparable effects on anti-CD40-activated B-CLL cells, which are blocked by anti-IL-4 receptor (IL-4R) monoclonal antibodies. However, IL-13-dependent effects are absent or inefficient in non-activated or anti-IgM-activated B-CLL cells. This suggests that such cells may lack functional IL-13 receptors, though IL-13R and IL-4R on B-CLL cells share a common component. [ABSTRACT FROM AUTHOR]