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Production by Peripheral Blood Mononuclear Cells in Response to Viral Stimulation1
*
Department of Pathology and Laboratory Medicine, and
Graduate School of Biomedical Sciences, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, NJ 07103
IL-10 is an important regulator of the production of
proinflammatory cytokines. Its effect on IFN-
production, however,
has not been reported. In this study, PBMC from healthy donors were
stimulated with virus in the presence of IL-10. Human IL-10 (hIL-10)
caused reductions in both the frequency of IFN--producing cells
(IPC) and bulk IFN in response to herpes simplex virus type-1 (HSV-1),
Sendai virus, Newcastle disease virus, and vesicular stomatitis virus.
The inhibitory effect occurred when IL-10 was added 2 or 4 h
before, or 2 h poststimulation with HSV or Sendai virus, but not
when added 4 h postinduction. Unlike IL-10, IL-4 did not affect
the IFN- response to HSV. However, when PBMC were induced with
Sendai virus, IFN- production was also reduced by IL-4. IL-10
treatment of PBMC resulted in strong reductions in the steady state
levels of both HSV- and Sendai virus-induced IFN-1, -2, and -ß
mRNA as determined by RT-PCR. IFN- production to Sendai virus occurs
predominantly by monocytes, whereas most enveloped viruses stimulate
low frequency "natural IFN-producing cells (NIPC)," which are
thought to be dendritic cells. Peripheral blood dendritic cells were
found to express the IL-10 receptor, suggesting that IL-10 may directly
act on the dendritic IPC. Addition of monoclonal anti-IL-10 to PBMC
resulted in a significant increase in both the frequency of IPC and the
amount of secreted IFN- in response to HSV but not Sendai virus. We
conclude that human IL-10 can serve as both an endogenous and exogenous
regulator of IFN- production.
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