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Lymphomagenesis in the SCID-hu mouse involves abundant production of human
interleukin-10
RA Baiocchi, ME Ross, JC Tan, CC Chou, L Sullivan, S Haldar, M Monne, MV Seiden, SK Narula and J Sklar
Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY.
Both human (hu) and viral (v) interleukin-10 (IL-10) appear to be important
cofactors in the survival and growth of lymphoblastoid cell lines infected
with Epstein-Barr virus (EBV). When mice with severe combined immune
deficiency (SCID) are injected with human peripheral blood lymphocytes
(PBL) from normal individuals who are seropositive for EBV, the majority of
hu-PBL-SCID mice will develop an EBV- associated lymphoproliferative
disease (EBV-LPD) of human B-cell origin, not unlike some cases of EBV-LPD
that are seen in immunocompromised individuals. The role of huIL-10 or
vIL-10 in this chimeric mouse model of EBV-LPD is unknown. In the present
study, we show that hu-PBL-SCID mice that develop EBV-LPD have significant
elevation of serum huIL-10 levels compared with mice that do not develop
EBV-LPD (P = .005). vIL-10 was undetectable in all animals. The EBV+ tumor
samples express transcript for huIL-10 and huIL-10 receptor, express
huIL-10 protein by immunohistochemical staining, and show specific binding
of recombinant (r) huIL-10. In vitro analysis of the functional
consequences of rhuIL-10 binding to IL-10 receptors on fresh EBV+ tumor
cells shows that rhuIL-10 can prevent programmed cell death as well as
promote proliferation and can do so at concentrations of huIL-10 found in
vivo. Thus, huIL-10 production by EBV+ tumor cells may contribute directly
to their malignant outgrowth in the hu-PBL-SCID mouse by two autocrine
mechanisms: prevention of programmed cell death and proliferation. The
implications of such findings with regard to EBV- LPD in humans is
discussed.
Volume 85,
Issue 4,
pp. 1063-1074,
02/15/1995
Copyright © 1995 by The American Society of Hematology
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