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Interleukin-13 inhibits interleukin-2-induced proliferation and protects
chronic lymphocytic leukemia B cells from in vitro apoptosis
N Chaouchi, C Wallon, C Goujard, G Tertian, A Rudent, D Caput, P Ferrera, A Minty, A Vazquez and JF Delfraissy
Laboratoire Virus Neurone et Immunite, Faculte de Medecine Paris Sud,
France.
Human interleukin-13 (IL-13) acts at different stages of the normal B- cell
maturation pathway with a spectrum of biologic activities overlapping those
of IL-4. B chronic lymphocytic leukemia (B-CLL) is characterized by the
accumulation of slow-dividing and long-lived monoclonal B cells, arrested
at the intermediate stage of their differentiation. In vitro, B-CLL cells
exhibit a spontaneous apoptosis regulated by different cytokines. In this
report, we show that IL-13 (10 to 200 ng/mL) acts directly on monoclonal
B-CLL cells from 12 patients. (1) IL-13 enhances CD23 expression and
induces soluble CD23 secretion by B-CLL cells but does not exhibit a growth
factor activity. (2) IL-13 inhibits IL-2 responsiveness of B-CLL cells,
activated either with IL-2 alone or through crosslinking of lgs or ligation
of CD40 antigen. (3) IL-13 protects B-CLL cells from in vitro spontaneous
apoptosis. The effects of IL-13 on neoplasic B cells were slightly less
than those of IL-4 and occurred independently of the presence of IL-4. The
present observations show that IL-13 may exhibit a negative regulatory
effect on neoplasic B cells in contrast with that observed in normal B
cells, and suggest that IL-13 could be an important factor in the
pathogenesis of CLL by preventing the death of monoclonal B cells.
Moreover, B-CLL may be an interesting model to study the regulation of the
expression of IL-13 receptor and/or signal transduction pathways.
Volume 87,
Issue 3,
pp. 1022-1029,
02/01/1996
Copyright © 1996 by The American Society of Hematology
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