The recently described interleukin-13 (IL-13) has been shown to share
many of the effects of IL-4 on normal B cells, including growth-promot
ing activity and induction of CD23. In this study, we compared the eff
ects of IL-13 and IL-4 on B chronic lymphocytic leukaemias (B-CLL) cel
ls. After anti-CD40 activation, both IL-13 and IL-4 promoted the DNA s
ynthesis of B-CLL cells and increased the recovery of viable cells. Th
e time kinetics of the proliferative response of B-CLL cells to IL-13
or IL-4 were superimposable and showed the long-lasting effect of both
cytokines. As on normal B cells, both IL-4 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 leukaemic B ce
lls. 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-IL-4 receptor monoclonal antibody, sugg
esting 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-driv
en proliferation of anti-IgM-activated B-CLL cells. Furthermore, while
IL-4 strongly up-regulated the expression of CD23 on anti-IgM-activat
ed leukaemic 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-CD4
0-activated B-CLL cells, which are blocked by anti-IL-4 receptor (IL-4
R) monoclonal antibodies. However, IL-13-dependent effects are absent
or inefficient in non-activated or anti-IgM-activated B-CLL cells. Thi
s suggests that such cells may lack functional IL-13 receptors, though
IL-13R and IL-4R on B-CLL cells share a common component.