Interleukin-5 (IL-5) increases spontaneous apoptosis of B-cell chronic
lymphocytic leukemia cells in vitro independently of bcl-2 expression and
is inhibited by IL-4
T Mainou-Fowler, VA Craig, JA Copplestone, MD Hamon and AG Prentice
Department of Haematology, Derriford Hospital, Plymouth, UK.
During hematopoiesis, viability factors that suppress apoptosis are
required throughout the differentiation process. Some of these factors may
also function as growth factors. Interleukin-5 (IL-5) is recognized as a
growth factor in hematopoiesis. We examined the involvement of IL- 5 as a
viability factor of B-CLL in vitro. In 13 B-CLL cases studied, IL-5 at 20
U/mL increased spontaneous apoptosis by a mean percentage of 53% (range,
20% to 129%) (P < .05) after 2 days in culture. On the third day, the
mean percentage increase was 37% (range, 18% to 50%). In all cases, IL-4
protected B-CLL cells against IL-5-induced apoptosis by a mean percentage
of 47% (range, 18% to 81%) (P < .001). This protection was specific to
IL-4 and it was reduced with anti-IL-4 antibody. In addition, expression of
bcl-2 protein in untreated cultures was not significantly different from
that of the IL-5-treated cells; mean equivalent of soluble fluorochrome
(MESF) was 5.2 (range, 3.0 to 6.8) and 4.9 (range, 3.0 to 6.3),
respectively (P > .2). In freshly isolated B-CLL cells, the MESF was 4.5
(range, 2.4 to 6.6). These results show that IL-5 induced apoptosis in
B-CLL cells by a pathway that is independent of bcl-2 expression. IL-4
partially protects against this effect.
Volume 84,
Issue 7,
pp. 2297-2304,
10/01/1994
Copyright © 1994 by The American Society of Hematology
