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Blood, 1 October 2000, Vol. 96, No. 7, pp. 2568-2573
NEOPLASIA
Abolished angiogenicity and tumorigenicity of Burkitt
lymphoma by interleukin-10
Laszlo Cervenak,
Lucia Morbidelli,
Daria Donati,
Sandra Donnini,
Taku Kambayashi,
Julia L. Wilson,
Håkan Axelson,
Esmeralda Castaños-Velez,
Hans-Gustaf Ljunggren,
Rene
De Waal Malefyt,
Harris J. Granger,
Marina Ziche, and
Maria Teresa Bejarano
From the Microbiology and Tumor Biology Center,
Karolinska Institutet, Stockholm, Sweden; the Institute of
Pharmacological Sciences, University of Siena, Italy; the Department of
Medicine, Division of Molecular Medicine, Lund University, Sweden; the
Immunopathology Laboratory, Cancer Center, Karolinska Hospital,
Stockholm, Sweden; the DNAX Research Institute, Palo Alto, CA; and the
Department of Medical Physiology and Cardiovascular Research Institute,
TX.
Because of its immunosuppressive properties, interleukin-10 (IL-10)
is thought to play an important role in a number of human disease
states, including inflammation, autoimmunity, and transplant rejection.
In this study, we demonstrate that introduction of human or viral IL-10
genes into Burkitt's lymphoma cells markedly reduced their ability to
grow as subcutaneous (sc) tumors in SCID mice. In vivo assays
for angiogenesis revealed an inhibition of the angiogenic capacity of
the IL-10-transfected lines. Recombinant human IL-10 abolished and
viral IL-10 reduced vascular endothelial growth factor
(VEGF)-165-induced neovascularization. Furthermore, IL-10 blocked the
VEGF- and fibroblast growth factor (FGF)-2-induced proliferation of
microvascular endothelial cells in vitro. The current observations
suggest a direct role for IL-10 in the prevention of angiogenesis in
human lymphoid malignancies.
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