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Interleukin-13 in combination with CD40 ligand potently inhibits apoptosis
in human B lymphocytes: upregulation of Bcl-xL and Mcl-1
J Lomo, HK Blomhoff, SE Jacobsen, S Krajewski, JC Reed and EB Smeland
Department of Immunology, Institute for Cancer Research, The Norwegian
Radium Hospital, Oslo.
Interleukin-13 (IL-13) is a novel T-cell-derived cytokine with IL-4- like
effects on many cell types. In human B lymphocytes, IL-13 induces
activation, stimulates proliferation in combination with anti-IgM or
anti-CD40 antibodies, and directs Ig isotype switching towards IgE and IgG4
isotypes. We show here that IL-13 also regulates human B-cell apoptosis.
IL-13 reduced spontaneous apoptosis of peripheral blood B cells in vitro,
as shown by measurement of DNA fragmentation using the TUNEL and Nicoletti
assays. The inhibition of cell death by IL-13 alone was significant but
modest, but was potently enhanced in combination with CD40 ligand (CD40L),
a survival stimulus for B cells by itself. Interestingly, IL-13 increased
the expression of CD40 on peripheral blood B cells, providing a possible
mechanism for the observed synergy. IL-13 alone was a less potent inhibitor
of apoptosis than IL-4. Moreover, there was no additive effect of combining
IL-4 and IL-13 at supraoptimal concentrations, which is consistent with the
notion that the IL-4 and IL-13 binding sites share a common signaling
subunit. The combination of IL-13 with CD40L augmented the expression of
the Bcl-2 homologues Bcl-xL and Mcl-1, suggesting this as a possible
intracellular mechanism of induced survival. By contrast, levels of Bcl- 2,
and two other Bcl-2 family members, Bax and Bak, remained unaltered. Given
the importance of the CD40-CD40L interaction in B-cell responses, these
results suggest a significant role of IL-13 in the regulation of B-cell
apoptosis.
Volume 89,
Issue 12,
pp. 4415-4424,
06/15/1997
Copyright © 1997 by The American Society of Hematology
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