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, A Novel Type I IFN, On Cytokine Production by Cells of the Innate Immune System
* Human Genome Sciences, Rockville, MD 20850; and
Istituto Dermopatico dell’Immacolata, Rome, Italy
IFN-
is a recently identified type I IFN that exhibits both
structural and functional homology with the other type I IFN
subclasses. In this study, we have investigated the effect of IFN-
on cells of the innate immune system by comparing cytokine release
following treatment of human cells with either IFN- or two
recombinant IFN subtypes, IFN-
and IFN-
2a. Although IFN-2a
failed to stimulate monocyte cytokine secretion, IFN-, like
IFN-, induced the release of several cytokines from both
monocytes and dendritic cells, without the requirement of a
costimulatory signal. IFN- was particularly effective in inhibiting
inducible IL-12 release from monocytes. Unlike IFN-, IFN- did not
induce release of IFN-
by PBL. Expression of the IFN- mRNA was
observed in resting dendritic cells and monocytes, and it was
up-regulated by IFN- stimulation in monocytes, while IFN- mRNA
was minimally detectable under the same conditions. Monocyte and
dendritic cell expression of IFN- was also confirmed in vivo
in chronic lesions of psoriasis vulgaris and atopic dermatitis.
Finally, biosensor-based binding kinetic analysis revealed that
IFN-, like IFN-, binds strongly to heparin
(Kd: 2.1 nM), suggesting that the cytokine
can be retained close to the local site of production. The pattern of
cytokines induced by IFN- in monocytes, coupled with the unique
induction of IFN- mRNA by IFN-, indicates a potential role for
IFN- in the regulation of immune cell
functions.
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