More MS news articles for September 2002

Cutting edge: oral type I IFN-tau promotes a Th2 bias and enhances suppression of autoimmune encephalomyelitis by oral glatiramer acetate

J Immunol 2002 Sep 1;169(5):2231-5
Soos JM, Stuve O, Youssef S, Bravo M, Johnson HM, Weiner HL, Zamvil SS.
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

IFN-tau, 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-tau alone and in combination with oral glatiramer acetate in experimental allergic encephalomyelitis (EAE).

By comparison of oral administration of IFN-alpha, -beta, and -tau 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-alpha and -beta induced IFN-gamma secretion, a Th1 cytokine, IFN-tau did not.

Oral IFN-tau alone suppressed EAE.

When suboptimal doses were administered orally in combination to wild-type mice, IFN-tau and glatiramer acetate had a synergistic beneficial effect in suppression of EAE.

This combination was associated with TGF-beta secretion and enhanced IL-10 production.

Thus, IFN-tau is a potential candidate for use as a single agent or in combination therapy for multiple sclerosis.