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Blood, Vol. 93 No. 5 (March 1), 1999:
pp. 1456-1463
Interleukin-10 Inhibits Expression of Both Interferon  - and
Interferon  - Induced Genes by Suppressing Tyrosine
Phosphorylation of STAT1
Satoshi Ito,
Parswa Ansari,
Minoru Sakatsume,
Harold Dickensheets,
Nancy Vazquez,
Raymond P. Donnelly,
Andrew C. Larner, and
David S. Finbloom
From Division of Cytokine Biology, Center for Biologics Evaluation
and Research, Food and Drug Administration, Bethesda, MD.
Interleukin-10 (IL-10) helps maintain polarized T-helper cells in a
T-helper lymphocyte 2 (Th2) phenotype. Part of this
process involves the prevention of the development of Th1 cells, which are a primary source of interferon  (IFN), a potent activator of
monocytes and an inhibitor of Th2 proliferation. Because monocytes and
macrophages are important mediators of Th1-type responses, such as
delayed-type hypersensitivity, we sought to determine if IL-10 could
directly mediate inhibition of IFN- and IFN -induced gene
expression in these cells. Highly purified monocytes were incubated
with IL-10 for 60 to 90 minutes before the addition of IFN or
IFN. IL-10 preincubation resulted in the inhibition of gene
expression for several IFN-induced genes, such as IP-10, ISG54, and
intercellular adhesion molecule-1. The reduction in gene expression
resulted from the ability of IL-10 to suppress IFN-induced assembly of
signal transducer and activator of transcription (STAT) factors to
specific promoter motifs on IFN- and IFN-inducible genes. This
was accomplished by preventing the IFN-induced tyrosine phosphorylation
of STAT1, a component of both IFN- and IFN-induced DNA binding
complexes. Therefore, IL-10 can directly inhibit STAT-dependent early
response gene expression induced by both IFN and IFN in monocytes
by suppressing the tyrosine phosphorylation of STAT1. This may occur
through the ability of IL-10 to induce expression of the gene,
suppressor of cytokine signaling 3 (SOCS3).
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