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Interleukin-10 suppresses human immunodeficiency virus-1 replication in
vitro in cells of the monocyte/macrophage lineage
MW Saville, K Taga, A Foli, S Broder, G Tosato and R Yarchoan
Retroviral Diseases Section, National Cancer Institute, Bethesda, MD 20892.
The cytokine interleukin-10 (IL-10) has been implicated in the pathogenesis
of a number of disease states, including Epstein-Barr virus and human
immunodeficiency virus (HIV-1) infections. In the acquired immunodeficiency
syndrome (AIDS), it has been suggested that IL-10 may have a deleterious
effect by suppressing cell-mediated immunity. However, there are few data
on its direct effects on HIV-1 replication. In the present study, we have
found that recombinant human IL-10 (rhIL-10), present during days 0 through
2, potently inhibits HIV production in elutriated monocyte/macrophage (M/M)
cultures with a 50% inhibitory concentration (IC50) of approximately 0.03
U/mL. This effect did not appear to be caused by toxicity to M/M because
there was no change in cell viability, ability to phagocytose latex beads,
or protein synthesis as measured by [3H]-leucine incorporation, at doses of
rhIL-10 that inhibit viral replication. In addition,
lipopolysaccharide-induced production of IL-1 beta, IL-6, or tumor necrosis
factor-alpha was not affected at these doses, nor were human mononuclear
cell proliferative responses to phytohemagglutinin, OKT3 antibody, or
tetanus toxoid. HIV-1 replication was similarly decreased by rhIL-10 in the
monocytoid line U937 without signs of cellular toxicity. However, these
effects required much higher concentrations of rhIL-10, and viral
production was only partially suppressed. rhIL-10 also slightly inhibited
HIV-induced cytopathicity in ATH-8, a tetanus toxoid-specific, retrovirally
immortalized T-cell line, but had no effect on HIV replication in the H9
and MOLT-4 T cell lines. Thus, rhIL- 10 appears to inhibit HIV replication
predominantly in cells of the M/M lineage. This effect may serve to reduce
viral production in patients with AIDS. However, additional studies will be
needed to more precisely define its physiologic role in this disease.
Volume 83,
Issue 12,
pp. 3591-3599,
06/15/1994
Copyright © 1994 by The American Society of Hematology
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