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Cutting Edge |
Promotes a Th2 Bias and Enhances Suppression of Autoimmune Encephalomyelitis by Oral Glatiramer Acetate1
* Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115;
Department of Neurology, University of California, San Francisco, CA 94143;
Department of Neurology, Stanford Medical School, Stanford, CA 94305; and
Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611
IFN-
, a novel type I IFN that possesses immunomodulatory
properties, lacks toxicity normally associated with other type I IFNs.
We examined the effects of oral IFN- alone and in combination with
oral glatiramer acetate in experimental allergic encephalomyelitis
(EAE). By comparison of oral administration of IFN-
, -
, and -
to myelin basic protein-specific TCR-transgenic mice, we demonstrate
these type I IFNs promote secretion of the Th2 cytokine IL-10 with
similar efficiency. Whereas IFN- and - induced IFN-
secretion,
a Th1 cytokine, IFN- did not. Oral IFN- alone suppressed EAE.
When suboptimal doses were administered orally in combination to
wild-type mice, IFN- and glatiramer acetate had a synergistic
beneficial effect in suppression of EAE. This combination was
associated with TGF- secretion and enhanced IL-10 production. Thus,
IFN- is a potential candidate for use as a single agent or in
combination therapy for multiple sclerosis.
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